coenzyme-q10 and Inflammation

Coenzyme Q10 (CoQ10) has become a popular nutritional supplement due to its wide range of beneficial biological effects. Previous meta-analyses show that the attenuation of CoQ10 on inflammatory biomarkers remains controversial. This meta-analysis aims to assess the efficacy and optimal dose of CoQ10 supplementation on inflammatory indicators in the general population.. Databases are searched up to December 2022 resulting in 6713 articles, of which 31 are retrieved for full-text assessment and included 1517 subjects. Double-blind randomized controlled trials (RCTs) of CoQ10 supplementation are eligible if they contain C reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). CoQ10 supplementation can significantly reduce the levels of circulating CRP (SMD: -0.40, 95% CI: [-0.67 to -0.13], p = 0.003), IL-6 (SMD: -0.67, 95% CI: [-1.01 to -0.33], p < 0.001), and TNF-α (SMD: -1.06, 95% CI: [-1.59 to -0.52], p < 0.001) and increase the concentration of circulating CoQ10.. This meta-analysis provides evidence for CoQ10 supplementation to reduce the level of inflammatory mediators in the general population and proposes that daily supplementation of 300-400 mg CoQ10 show superior inhibition of inflammatory factors.

Topics: Biomarkers; C-Reactive Protein; Dietary Supplements; Humans; Inflammation; Interleukin-6; Randomized Controlled Trials as Topic; Tumor Necrosis Factor-alpha; Ubiquinone

COPD represents a major cause of mortality and morbidity worldwide, is linked to systemic inflammation and tends to coexist with a variety of comorbidities. Inflammation, oxidative stress and protease-antiprotease imbalance represent the pathogenic triad of COPD. Even though oxidative stress and mitochondrial dysfunction is a well-studied phenomenon in COPD and there is a variety of studies that aim to counteract its effect, there is limited data available on the use of coenzyme Q10 in COPD. The aim of the current review is to analyze the current data on the use of coenzyme Q10 in the management of COPD and frequently encountered comorbidities.

Topics: Humans; Inflammation; Oxidative Stress; Pulmonary Disease, Chronic Obstructive; Ubiquinone

Systemic inflammation and oxidative stress (OS) are associated with breast cancer. CoQ10 as an adjuvant treatment with conventional anti-cancer chemotherapy has been demonstrated to help in the inflammatory process and OS. This systematic review and meta-analysis of randomized clinical trials (RCTs) aimed to evaluate the efficacy of CoQ10 supplementation on levels of inflammatory markers, OS parameters, and matrix metalloproteinases/tissue inhibitor of metalloproteinases (MMPs/TIMPs) in patients with breast cancer.. A systematic literature search was carried out using electronic databases, including PubMed, Web of Science, Scopus, Google Scholar, and Embase, up to December 2020 to identify eligible RCTs evaluating the effect of CoQ10 supplementation on OS biomarkers, inflammatory cytokines, and MMPs/TIMPs. From 827 potential reports, 5 eligible studies consisting of 9 trials were finally included in the current meta-analysis. Quality assessment and heterogeneity tests of the selected trials were performed using the PRISMA checklist protocol and the I. Overall, the findings showed that CoQ10 supplementation reduced some of the important markers of inflammation and MMPs in patients with breast cancer. However, further studies with controlled trials for other types of cancer are needed to better understand and confirm the effect of CoQ10 on tumor therapy.

Topics: Angiogenesis Inhibitors; Breast Neoplasms; Dietary Supplements; Female; Humans; Inflammation; Inflammation Mediators; Matrix Metalloproteinase Inhibitors; Matrix Metalloproteinases; Oxidative Stress; Randomized Controlled Trials as Topic; Tissue Inhibitor of Metalloproteinases; Treatment Outcome; Ubiquinone

Evidence from randomized controlled trials (RCTs) suggests that coenzyme Q

Topics: Adipokines; Animals; Biomarkers; Dietary Supplements; Disease Management; Disease Susceptibility; Humans; Inflammation; Lipid Peroxidation; Metabolic Syndrome; Oxidative Stress; Publication Bias; Ubiquinone

Coenzyme Q10 (CoQ10) has a number of vital functions in all cells, both mitochondrial and extramitochondrial. In addition to its key role in mitochondrial oxidative phosphorylation, CoQ10 serves as a lipid soluble antioxidant, plays an important role in fatty acid, pyrimidine and lysosomal metabolism, as well as directly mediating the expression of a number of genes, including those involved in inflammation. In view of the central role of CoQ10 in cellular metabolism, it is unsurprising that a CoQ10 deficiency is linked to the pathogenesis of a range of disorders. CoQ10 deficiency is broadly classified into primary or secondary deficiencies. Primary deficiencies result from genetic defects in the multi-step biochemical pathway of CoQ10 synthesis, whereas secondary deficiencies can occur as result of other diseases or certain pharmacotherapies. In this article we have reviewed the clinical consequences of primary and secondary CoQ10 deficiencies, as well as providing some examples of the successful use of CoQ10 supplementation in the treatment of disease.

Topics: Antioxidants; Ataxia; Humans; Inflammation; Mitochondrial Diseases; Muscle Weakness; Ubiquinone

SARS-CoV-2 causes a severe pneumonia (COVID-19) that affects essentially elderly people. In COVID-19, macrophage infiltration into the lung causes a rapid and intense cytokine storm leading finally to a multi-organ failure and death. Comorbidities such as metabolic syndrome, obesity, type 2 diabetes, lung and cardiovascular diseases, all of them age-associated diseases, increase the severity and lethality of COVID-19. Mitochondrial dysfunction is one of the hallmarks of aging and COVID-19 risk factors. Dysfunctional mitochondria is associated with defective immunological response to viral infections and chronic inflammation. This review discuss how mitochondrial dysfunction is associated with defective immune response in aging and different age-related diseases, and with many of the comorbidities associated with poor prognosis in the progression of COVID-19. We suggest here that chronic inflammation caused by mitochondrial dysfunction is responsible of the explosive release of inflammatory cytokines causing severe pneumonia, multi-organ failure and finally death in COVID-19 patients. Preventive treatments based on therapies improving mitochondrial turnover, dynamics and activity would be essential to protect against COVID-19 severity.

Topics: Aging; Animals; COVID-19; Cytokine Release Syndrome; Humans; Inflammation; Mitochondria; SARS-CoV-2; Ubiquinone

Systemic inflammation and oxidative stress significantly contribute in developing coronary artery disease (CAD). This systematic review and meta-analysis was aimed to determine the effects of coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress among patients with CAD.. The electronic databases including MEDLINE, EMBASE, Scopus, Web of Science, and Cochrane Library databases were systematically searched until Oct 2018. The quality assessment and heterogeneity of the selected randomized clinical Trials (RCTs) were examined using the Cochrane Collaboration risk of bias tool, and Q and I. Overall, this meta-analysis demonstrated CoQ10 supplementation increased SOD and CAT, and decreased MDA and diene levels, but did not affect CRP, TNF-α, IL-6, and GPx levels among patients with CAD.

Topics: Animals; Biomarkers; Coronary Artery Disease; Dietary Supplements; Humans; Inflammation; Oxidative Stress; Randomized Controlled Trials as Topic; Ubiquinone

Systematic inflammation plays a major role in all stages of chronic diseases. Recent evidence suggests that Coenzyme Q10 (CoQ10), as an anti-inflammatory agent, has shown beneficial effects on the inflammatory process of various human diseases. However, several trials have examined the effects of CoQ10 on pro-inflammatory cytokines with contrasting results. The objective of this systematic review and meta-analysis of randomized clinical trials (RCTs) was to assess the efficacy of CoQ10 supplementation on tumor necrosis factor- α (TNF-α) and interleukin-6 (IL-6) levels.. A systematic literature was performed on databases including PubMed/Medline, EMBASE, Web of Science, SCOPUS, Cochrane Library databases, Clinical Trials.gov and historical search of reference lists from selected studies up to December 2018. Two reviewers independently investigated study eligibility, extracted data, and assessed risk of bias of relevant studies using a standardized protocol. Heterogeneity was measured by the I. Overall, nine RCTs with a total of 509 patients (269 in the CoQ10 arm and 240 in the control arm) provided the inclusion criteria and were included in the analysis. Our meta-analysis indicated that oral CoQ10 supplementation (60-500 mg/day for 8-12 weeks) resulted in significant reduction of TNF-α (SMD: -0.44, 95% CI: [-0.81 to -0.07] mg/dl; I. This meta-analysis of RCTs reported a significant effect of CoQ10 on some of the inflammatory markers among patients with chronic diseases which could attenuate the inflammatory state. However, well-designed studies with a larger sample size are required. Note that the results should be interpreted with caution because of the evidence of heterogeneity and limited number of studies.

Topics: Anti-Inflammatory Agents; Dietary Supplements; Humans; Inflammation; Interleukin-6; Randomized Controlled Trials as Topic; Tumor Necrosis Factor-alpha; Ubiquinone

Chronic inflammation contributes to the onset and development of metabolic diseases. Clinical evidence has suggested that coenzyme Q10 (CoQ10) has some effects on inflammatory markers. However, these results are equivocal. The aim of this systematic review was to assess the effects of CoQ10 on serum levels of inflammatory markers in people with metabolic diseases.. Electronic databases were searched up to February 2016 for randomized controlled trials (RCTs). The outcome parameters were related to inflammatory factors, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and C reactive protein (CRP). RevMan software was used for meta-analysis. Meta-regression analysis, Egger line regression test and Begg rank correlation test were performed by STATA software.. Nine trials involving 428 subjects were included in this meta-analysis. The results showed that compared with control group, CoQ10 supplementation has significantly improved the serum level of CoQ10 by 1.17μg/ml [MD = 1.17, 95% CI (0.47 to 1.87) μg/ml, I2 = 94%]. Meanwhile, it has significantly decreased TNF-α by 0.45 pg/ml [MD = -0.45, 95% CI (-0.67 to -0.24) pg/ml, I2 = 0%]. No significant difference was observed between CoQ10 and placebo with regard to CRP [MD = -0.21, 95% CI (-0.60 to 0.17) mg/L, I2 = 21%] and IL-6 [MD = -0.89, 95% CI (-1.95 to 0.16) pg/ml, I2 = 84%].. CoQ10 supplementation may partly improve the process of inflammatory state. The effects of CoQ10 on inflammation should be further investigated by conducting larger sample size and well-defined trials of long enough duration.

Topics: Biomarkers; C-Reactive Protein; Dietary Supplements; Electronic Health Records; Humans; Inflammation; Interleukin-6; Randomized Controlled Trials as Topic; Tumor Necrosis Factor-alpha; Ubiquinone

Atherothrombosis is a recurrent complication in APS and SLE patients. Oxidative stress has been suggested as a key player underlying this process. Autoantibodies have been pointed to as the main contributors to abnormality in the oxidative status observed in APS and SLE patients, promoting the increased production of oxidant species and the reduction of antioxidant molecules. This imbalance causes vascular damage through the activation of immune cells, including monocytes, lymphocytes and neutrophils, causing the expression of pro-inflammatory and procoagulant molecules, the formation of neutrophil extracellular traps and the adhesion of these cells to the endothelium; the induction of cellular apoptosis and impaired cell clearance, which in turn enhances autoantibody neogeneration; and cytotoxicity of endothelial cells. This review describes the mechanisms underlying the role of oxidative stress in the pathogenesis of atherothrombosis associated with APS and SLE, focused on the effect of autoantibodies, the different cell types involved and the diverse effectors, including cytokines, procoagulant proteins and their main modulators, such as oxidant/antioxidant species and intracellular pathways in each pathology. We further discuss new therapies aimed at restoring the oxidative stress balance and subsequently to tackle atherothrombosis in APS and SLE.

Topics: Acetylcysteine; Anticoagulants; Antioxidants; Antiphospholipid Syndrome; Atherosclerosis; Autoantibodies; beta 2-Glycoprotein I; Coagulants; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Inflammation; Lupus Erythematosus, Systemic; Mitochondrial Diseases; Oxidative Stress; Reactive Oxygen Species; Recurrence; Thrombosis; Ubiquinone

The aging risk factor for Parkinson's disease is described in terms of specific disease markers including mitochondrial and gene dysfunctions relevant to energy metabolism. This review details evidence for the ability of nutritional agents to manage these aging risk factors. The combination of alpha lipoic acid, acetyl-l-carnitine, coenzyme Q10, and melatonin supports energy metabolism via carbohydrate and fatty acid utilization, assists electron transport and adenosine triphosphate synthesis, counters oxidative and nitrosative stress, and raises defenses against protein misfolding, inflammatory stimuli, iron, and other endogenous or xenobiotic toxins. These effects are supported by gene expression via the antioxidant response element (ARE; Keap/Nrf2 pathway), and by peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1 alpha), a transcription coactivator, which regulates gene expression for energy metabolism and mitochondrial biogenesis, and maintains the structural integrity of mitochondria. The effectiveness and synergies of the combination against disease risks are discussed in relation to gene action, dopamine cell loss, and the accumulation and spread of pathology via misfolded alpha-synuclein. In addition there are potential synergies to support a neurorestorative role via glial derived neurotrophic factor expression.

Topics: Acetylcarnitine; Adenosine Triphosphate; Aging; alpha-Synuclein; Antioxidant Response Elements; Carbohydrate Metabolism; Electron Transport; Energy Metabolism; Fatty Acids; Glial Cell Line-Derived Neurotrophic Factor; Humans; Inflammation; Melatonin; Mitochondria; Nitric Oxide; Oxidative Stress; Parkinson Disease; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Proteostasis Deficiencies; Risk Factors; Thioctic Acid; Transcription Factors; Ubiquinone

Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the degeneration and progressive loss of dopaminergic neurons in the substantia nigra pars compacta. It has been suggested that oxidative stress plays a role in the etiology and progression of PD. For instance, low levels of endogenous antioxidants, increased reactive species, augmented dopamine oxidation, and high iron levels have been found in brains from PD patients. In vitro and in vivo studies of Parkinson models evaluating natural and endogenous antioxidants such as polyphenols, coenzyme Q10, and vitamins A, C, and E have shown protective effects against oxidative-induced neuronal death. In this paper, we will review the mechanisms by which polyphenols and endogenous antioxidants can produce protection. Some of the mechanisms reviewed include: scavenging nitrogen and oxygen reactive species, regulation of signaling pathways associated with cell survival and inflammation, and inhibition of synphilin-1 and alpha-synuclein aggregation.

Topics: alpha-Synuclein; Animals; Antioxidants; Ascorbic Acid; Carrier Proteins; Cell Death; Dopamine; Dopaminergic Neurons; Humans; Inflammation; Nerve Tissue Proteins; Oxidation-Reduction; Oxidative Stress; Parkinson Disease; Polyphenols; Reactive Oxygen Species; Signal Transduction; Substantia Nigra; Ubiquinone; Vitamin A; Vitamin E

Pathological hallmarks of Parkinson's disease are destruction of dopaminergic neurons in the basal ganglia, especially the substantia nigra, and the presence of Lewy bodies within nerve cells. Environmental toxins are associated with the disease and, in a minority of cases, genetic factors have been identified. Inflammation-with activation of phagocytic microglia, release of cytokines, invasion by T cells, and complement activation-plays a role in damaging these neurons. Excessive production of reactive oxygen species, mitochondrial dysfunction leading to apoptosis, accumulation and oligomerization of the protein alpha-synuclein, and defective protein disposal by the ubiquitin proteasome system are involved in the complex web of events mediating nigral cell demise. Two agents of current interest, coenzyme Q10 and creatine, may be disease modifying, and large studies are in progress. Related mechanisms of other substances, including omega-3 fatty acids and vitamin D, are included in this review. The association with serum cholesterol levels and the effects of statin drugs are uncertain but important.

Topics: Anti-Inflammatory Agents; Cholesterol; Creatine; Diet Therapy; Fatty Acids, Omega-3; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Inflammation; Mitochondria; Neuroprotective Agents; Parkinson Disease; Ubiquinone; Vitamin D; Vitamins

The pathogenesis of Parkinson's disease (PD) remains obscure, but there is increasing evidence that impairment of mitochondrial function, oxidative damage, and inflammation are contributing factors. The present paper reviews the experimental and clinical evidence implicating these processes in PD. There is substantial evidence that there is a deficiency of complex I activity of the mitochondrial electron transport chain in PD. There is also evidence for increased numbers of activated microglia in both PD postmortem tissue as well as in animal models of PD. Impaired mitochondrial function and activated microglia may both contribute to oxidative damage in PD. A number of therapies targeting inflammation and mitochondrial dysfunction are efficacious in the MPTP model of PD. Of these, coenzyme Q(10) appears to be particularly promising based on the results of a recent phase 2 clinical trial in which it significantly slowed the progression of PD.

Topics: Animals; Anti-Inflammatory Agents; Coenzymes; Creatine; Disease Models, Animal; Free Radicals; Humans; Inflammation; Mitochondria; Oxidative Stress; Parkinson Disease; Ubiquinone

Evaluating the impact of coenzyme Q10 (CoQ10) supplementation on hormonal indices, mental health, and biomarkers of inflammatory responses and oxidative stress among female patients suffering from polycystic ovary syndrome (PCOS).. The present double-blinded, placebo-controlled randomized clinical trial consisted of 55 PCOS women (aged 18-40 years old), who were randomized into groups receiving 100 mg/day of CoQ10 (28 cases) or placebo (27 cases) for 12 weeks.. The supplementation of CoQ10 decreased significantly the scores of Beck Depression Inventory (BDI) (. 12-week supplementation of CoQ10 to PCOS women showed beneficial impact on BDI, BAI, hs-CRP, total testosterone, DHEAS, hirsutism, SHBG, TAC and MDA levels.

Topics: Adolescent; Adult; Antioxidants; Anxiety; Biomarkers; C-Reactive Protein; Dehydroepiandrosterone Sulfate; Depression; Dietary Supplements; Double-Blind Method; Female; Hirsutism; Humans; Inflammation; Mental Health; Metabolome; Oxidative Stress; Polycystic Ovary Syndrome; Sex Hormone-Binding Globulin; Testosterone; Ubiquinone; Young Adult

Selenium and coenzyme Q10 have synergistic antioxidant functions. In a four-year supplemental trial in elderly Swedes with a low selenium status, we found improved cardiac function, less cardiac wall tension and reduced cardiovascular mortality up to 12 years of follow-up. Here we briefly review the main results, including those from studies on biomarkers related to cardiovascular risk that were subsequently conducted. In an effort, to explain underlying mechanisms, we conducted a structured analysis of the inter-relationship between biomarkers.. Selenium yeast (200 µg/day) and coenzyme Q10 (200 mg/ day), or placebo was given to 443 elderly community-living persons, for 48 months. Structural Equation Modelling (SEM) was used to investigate the statistical inter-relationships between biomarkers related to inflammation, oxidative stress, insulin-like growth factor 1, expression of microRNA, fibrosis, and endothelial dysfunction and their impact on the clinical effects. The main study was registered at Clinicaltrials.gov at 30th of September 2011, and has the identifier NCT01443780.. In addition to positive clinical effects, the intervention with selenium and coenzyme Q10 was also associated with favourable effects on biomarkers of cardiovascular risk. Using these results in the SEM model, we showed that the weights of the first-order factors inflammation and oxidative stress were high, together forming a second-order factor inflammation/oxidative stress influencing the factors, fibrosis (β = 0.74; p < 0.001) and myocardium (β = 0.65; p < 0.001). According to the model, the intervention impacted fibrosis and myocardium through these factors, resulting in improved cardiac function and reduced CV mortality.. Selenium reduced inflammation and oxidative stress. According to the SEM analysis, these effects reduced fibrosis and improved myocardial function pointing to the importance of supplementation in those low on selenium and coenzyme Q10.

Topics: Aged; Biomarkers; Cardiovascular Diseases; Dietary Supplements; Double-Blind Method; Fibrosis; Humans; Inflammation; Latent Class Analysis; Oxidative Stress; Prospective Studies; Selenium; Sweden; Ubiquinone

This study aimed at determining the effects of coenzyme Q10 (CoQ10) supplementation on the inflammatory and endothelial dysfunction indices among overweight and obese women with polycystic ovary syndrome (PCOS).. This randomized double-blind, placebo-controlled clinical trial was performed among overweight and obese women diagnosed with PCOS. Forty three PCOS women were randomly assigned to two groups: one group received 200 mg CoQ10 capsules per day (. At the end of study, compared with pldacebo, CoQ10 supplementation resulted in significant decreases in serum levels of TNF-α (. The present study showed that CoQ10 supplementation for 8 weeks had a beneficial effect on inflammatory and endothelial dysfunction markers in overweight and obese patients with PCOS.

Topics: Adult; Biomarkers; Dietary Supplements; Double-Blind Method; Endothelium, Vascular; Female; Humans; Inflammation; Obesity; Polycystic Ovary Syndrome; Ubiquinone; Vitamins; Young Adult

Topics: Adult; Biomarkers; Curcumin; Dietary Supplements; Double-Blind Method; Female; Humans; Inflammation; Male; Migraine Disorders; Neuroprotective Agents; Oxidative Stress; Quality of Life; Ubiquinone

This study aimed to evaluate the effect of Coenzyme Q10 (CoQ10) administration to patients in the early phase of sepsis to determine its effect on the markers of inflammation and the clinical outcomes of septic patients.. Previous studies showed that CoQ10 levels were decreased in septic patients and worsening of mitochondrial dysfunction was observed.. In this randomized controlled trial septic patients (n=40) received 100 mg CoQ10 twice a day for seven days added to standard treatment of sepsis. As a primary endpoint levels of Interleukin 6 (IL-6), Tumor Necrosis Factor-α (TNF-α), Glutathione peroxidase and malondialdehyde (MDA) were assessed at baseline, third and 7th day after the intervention. Secondary endpoints included assessment of clinical scores and     in-hospital mortality.. There was no difference in baseline inflammatory and oxidative injury markers between the groups. TNF-α and MDA levels decreased significantly in the CoQ10 group on the 7th day of the study (P:0.003 for both). There was a significant difference in the in-hospital mortality in the CoQ10 group compared to the control group (P:0.01).. These findings suggest that CoQ10 has a positive effect on clinical parameters as well as mitochondrial dysfunction when administered in the early phase of sepsis (Tab. 2, Fig. 1, Ref. 38).

Topics: Biomarkers; Double-Blind Method; Humans; Inflammation; Malondialdehyde; Sepsis; Ubiquinone

The goal of this investigation was to determine if acute influenza infection is associated with depletion of CoQ10 compared to healthy controls and to determine any associations between CoQ10 levels and illness severity and inflammatory biomarkers.. We analyzed serum CoQ10 concentrations of patients with acute influenza enrolled in a randomized clinical trial prior to study drug administration. Patients were enrolled at a single urban tertiary care center over 3 influenza seasons (December 27, 2013 to March 31, 2016). Wilcoxon rank sum test was used to compare CoQ10 levels between influenza patients and healthy controls. Correlations with inflammatory biomarkers and severity of illness were assessed using Spearman correlation coefficient.. We analyzed CoQ10 levels from 50 patients with influenza and 29 controls. Overall, patients with acute influenza had lower levels of CoQ10 (.53 μg/mL, IQR .37-.75 vs .72, IQR .58-.90, P = .004). Significantly more patients in the influenza group had low CoQ10 levels (<.5 μg/mL) compared to controls (48% vs 7%, P < .001). Among influenza patients, there were significant but weak correlations between CoQ10 levels and IL-2 (r = -.30, P = .04), TNF-alpha (r = -.35, P = .01) and VEGF (r = .38, P = .007), but no correlation with IL-6, IL-10, VCAM or influenza severity of illness score (all P > .05).. We found that CoQ10 levels were significantly lower in patients with acute influenza infection and that these levels had significant although weak correlations with several inflammatory biomarkers.

Topics: Acute Disease; Adult; Atorvastatin; Biomarkers; Double-Blind Method; Female; Humans; Inflammation; Influenza, Human; Male; Middle Aged; Severity of Illness Index; Statistics, Nonparametric; Tertiary Care Centers; Ubiquinone; Young Adult

Atherosclerosis is a major risk factor for cardiovascular disease (CVD) and is known to be an inflammatory process. Statin therapy decreases both cholesterol and inflammation and is used in primary and secondary prevention of CVD. However, a statin induced decrease of plasma concentrations of the antioxidant coenzyme Q10 (CoQ10), may prevent the patients from reaching their optimal anti-inflammatory potential. Here, we studied the anti-inflammatory effect of Simvastatin therapy and CoQ10 supplementation.. 35 patients in primary prevention with Simvastatin (40 mg/day) were randomized to receive oral CoQ10 supplementation (400 mg/d) or placebo for 8 weeks. 20 patients with hypercholesterolemia who received no cholesterol-lowering treatment was a control group. Plasma concentrations of lipids and inflammatory biomarkers (interleukin-6 (IL6); -8 (IL8); -10 (IL10), tumor necrosis factor-α (TNFα); high-sensitivity C reactive protein (hsCRP)) as well as glycated hemoglobin (HbA1c) were quantified before and after the intervention.. No significant change in inflammatory markers or lipids was observed after CoQ10 supplementation Patients in Simvastatin therapy had significantly (P < 0.05) lower baseline concentration of IL6 (0.31 ± 0.03 pg/ml), IL8 (1.6 ± 0.1 pg/ml) IL10 (0.16 ± 0.02 pg/ml) and borderline (P = 0.053) lower TNFα (0.88 ± 0.05 pg/ml), but not hsCRP (1.34 ± 0.19 mg/l) compared with the control group (0.62 ± 0.08, 2.6 ± 0.2, 0.25 ± 0.01, 1.07 ± 0.09, and 1.90 ± 0.35, respectively).. Simvastatin therapy has beneficial effects on inflammatory markers in plasma, but CoQ10 supplementation seems to have no additional potentiating effect in patients in primary prevention. In contrast, glucose homeostasis may improve with CoQ10 supplementation.

Topics: Adult; Aged; Atherosclerosis; Biomarkers; C-Reactive Protein; Cytokines; Double-Blind Method; Female; Glycated Hemoglobin; Humans; Inflammation; Male; Middle Aged; Simvastatin; Ubiquinone

Although coenzyme Q10 (CoQ10) supplementation has shown to reduce pain levels in chronic pain, the effects of CoQ10 supplementation on pain, anxiety, brain activity, mitochondrial oxidative stress, antioxidants, and inflammation in pregabalin-treated fibromyalgia (FM) patients have not clearly elucidated. We hypothesised that CoQ10 supplementation reduced pain better than pregabalin alone

Topics: Adult; Brain; Double-Blind Method; Female; Fibromyalgia; Humans; Inflammation; Leukocytes, Mononuclear; Male; Middle Aged; Mitochondria; Oxidative Stress; Pain; Positron-Emission Tomography; Pregabalin; Ubiquinone

This research was conducted to assess the effects of coenzyme Q10 (CoQ10) intake on gene expression related to insulin, lipid and inflammation in subjects with polycystic ovary syndrome (PCOS).. This randomized double-blind, placebo-controlled trial was conducted on 40 subjects diagnosed with PCOS. Subjects were randomly allocated into two groups to intake either 100 mg CoQ10 (n = 20) or placebo (n = 20) per day for 12 weeks. Gene expression related to insulin, lipid and inflammation were quantified in blood samples of PCOS women with RT-PCR method.. Results of RT-PCR shown that compared with the placebo, CoQ10 intake downregulated gene expression of oxidized low-density lipoprotein receptor 1 (LDLR) (p < 0.001) and upregulated gene expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) (p = 0.01) in peripheral blood mononuclear cells of subjects with PCOS. In addition, compared to the placebo group, CoQ10 supplementation downregulated gene expression of interleukin-1 (IL-1) (p = 0.03), interleukin-8 (IL-8) (p = 0.001) and tumor necrosis factor alpha (TNF-α) (p < 0.001) in peripheral blood mononuclear cells of subjects with PCOS.. Overall, CoQ10 intake for 12 weeks in PCOS women significantly improved gene expression of LDLR, PPAR-γ, IL-1, IL-8 and TNF-α.

Topics: Adult; Dietary Supplements; Double-Blind Method; Female; Gene Expression; Gene Expression Regulation; Humans; Inflammation; Insulin; Interleukin-1; Interleukin-8; Leukocytes, Mononuclear; Lipid Metabolism; Polycystic Ovary Syndrome; PPAR gamma; Receptors, Oxidized LDL; Tumor Necrosis Factor-alpha; Ubiquinone

It has been reported that higher levels of oxidative stress and inflammation play a key role in the progression of hepatocellular carcinoma (HCC) after surgery. Coenzyme Q10 is an endogenous lipid-soluble antioxidant. To date, no intervention study has investigated coenzyme Q10 supplementation in HCC patients after surgery. The purpose of this study was to investigate oxidative stress, antioxidant enzymes activity, and inflammation levels in HCC patients after surgery following administration of coenzyme Q10 (300 mg/day).. This study was designed as a single-blinded, randomized, parallel, placebo-controlled study. Patients who were diagnosed with primary HCC (n = 41) and were randomly assign to a placebo (n = 20) or coenzyme Q10 (300 mg/day, n = 21) group after surgery. The intervention lasted for 12 weeks. Plasma coenzyme Q10, vitamin E, oxidative stress antioxidant enzymes activity and inflammatory markers levels were measured.. The oxidative stress (p = 0.04) and inflammatory markers (hs-CRP and IL-6, p < 0.01) levels were significantly decreased, and the antioxidant enzymes activity was significantly increased (p < 0.01) after 12 weeks of coenzyme Q10 supplementation. In addition, the coenzyme Q10 level was significantly negatively correlated with the oxidative stress (p = 0.01), and positively correlated with antioxidant enzymes activity (SOD, p = 0.01; CAT, p < 0.05; GPx, p = 0.04) and vitamin E level (p = 0.01) after supplementation.. In conclusion, we demonstrated that a dose of 300 mg/d of coenzyme Q10 supplementation significantly increased the antioxidant capacity and reduced the oxidative stress and inflammation levels in HCC patients after surgery.. Clinical Trials.gov Identifier: NCT01964001.

Topics: Aged; Antioxidants; Biomarkers; Body Mass Index; Body Weight; C-Reactive Protein; Carcinoma, Hepatocellular; Catalase; Dietary Supplements; Female; Humans; Inflammation; Interleukin-6; Linear Models; Liver Neoplasms; Male; Malondialdehyde; Middle Aged; Oxidative Stress; Single-Blind Method; Superoxide Dismutase; Ubiquinone; Vitamin E

Multiple sclerosis (MS) is an immune-mediated neurodegenerative disease of central nervous system and recent studies show that inflammatory processes are highly associated with neurodegeneration in the brain. The purpose of this study was to investigate the effect of coenzyme Q10 supplementation on inflammatory and anti-inflammatory markers in patients with MS.. This randomized, double-blind, placebo-controlled clinical study was performed among 48 patients with relapsing-remitting MS. Subjects were randomly assigned to a placebo group (n = 24) or coenzyme Q10 (CoQ10)-supplemented group (500 mg/day, n = 24). The intervention was administered for 12 weeks. Peripheral blood samples were collected at baseline and after 12-week intervention, to measure inflammatory (tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and matrix metalloproteinase (MMP)-9) and anti-inflammatory (IL-4 and TGF-β) markers.. Forty-five patients completed the study. After 12 weeks of intervention, the TNF-α levels (P = 0.003) decreased significantly in the CoQ10 group. Subjects in the CoQ10 group had significantly lower IL-6 levels (P = 0.037), compared to the placebo group. CoQ10 supplementation also resulted in decreased serum levels of MMP-9 as compared to the placebo group (P = 0.011). However, CoQ10 supplementation did not alter the IL-4 and TGF-β levels (P = 0.16 and P = 0.81, respectively).. CoQ10 supplementation at a dosage of 500 mg appears to decrease the inflammatory markers (TNF-α, IL-6, and MMP-9) in patients with MS.

Topics: Adult; Biomarkers; Dietary Supplements; Double-Blind Method; Female; Humans; Inflammation; Interleukin-4; Interleukin-6; Male; Matrix Metalloproteinases; Middle Aged; Multiple Sclerosis, Relapsing-Remitting; Transforming Growth Factor beta; Tumor Necrosis Factor-alpha; Ubiquinone

This study examined changes in toll-like receptor 4 (TLR-4)-expressing monocytes and lymphocyte subpopulations in response to continuous intensive exercise training in athletes, as well as the effect of coenzyme Q10 (CoQ10) supplementation on these changes. Eighteen male elite kendo athletes in Japan were randomly assigned to a CoQ10-supplementation group (n = 9) or a placebo-supplementation group (n = 9) using a double-blind method. Subjects in the CoQ10 group took 300 mg CoQ10 per day for 20 days. Subjects in the placebo group took the same dosage of placebo. All subjects practiced kendo 5.5 h per day for 6 consecutive days during the study period. Blood samples were collected 2 weeks before training, on the first day (day 1), third day (day 3), and fifth day of training (day 5), and 1 week after the training period (post-training) to ascertain TLR-4(+)/CD14(+) monocyte and lymphocyte subpopulations (CD3(+), CD4(+), CD8(+), CD28(+)/CD4(+), CD28(+)/CD8(+), and CD56(+)/CD3(-) cells) using flow cytometry analysis. The group × time interaction for TLR-4(+)/CD14(+) cells did not reach significance (p = 0.08). Within the CoQ10 group, the absolute number of TLR-4(+)/CD14(+) cells was significantly higher only at day 5. The placebo group showed a significant increase in the absolute number of TLR-4(+)/CD14(+) cells at day 3, day 5, and post-training (p < 0.05). There was no significant group × time interaction for any lymphocyte subpopulation. CD3(+), CD8(+), and CD56(+)/CD3(-) cells were significantly reduced at day 3 in both groups (p < 0.05). In conclusion, CoQ10 supplementation might downregulate the increase of TLR-4-expressing monocytes in response to continuous strenuous exercise training in kendo athletes.

Topics: Adipose Tissue; Athletes; Body Composition; Body Mass Index; Chronic Disease; Dietary Supplements; Double-Blind Method; Down-Regulation; Fatigue; Humans; Inflammation; Lymphocyte Subsets; Male; Martial Arts; Monocytes; Physical Endurance; Sports Nutritional Physiological Phenomena; Toll-Like Receptor 4; Ubiquinone; Young Adult

Inflammation and oxidative stress are central in many disease states. The major anti-oxidative enzymes contain selenium. The selenium intake in Europe is low, and supplementation with selenium and coenzyme Q10, important anti-oxidants, was evaluated in a previous study. The aim of this study was to evaluate response on the inflammatory biomarkers C-reactive protein, and sP-selectin, and their possible impact on cardiovascular mortality.. 437 elderly individuals were included in the study. Clinical examination, echocardiography, electrocardiography and blood samples were drawn. The intervention time was 48 months, and median follow-up was 5.2 years. The effects on inflammation/atherosclerosis were evaluated through analyses of CRP and sP-selectin. Evaluations of the effect of the intervention was performed using repeated measures of variance. All mortality was registered, and endpoints of mortality were assessed by Kaplan-Meier plots.. The placebo group showed a CRP level of 4.8 ng/mL at the start, and 5.1 ng/mL at the study end. The active supplementation group showed a CRP level of 4.1 ng/mL at the start, and 2.1 ng/mL at the study end. SP-selectin exhibited a level of 56.6 mg/mL at the start in the placebo group and 72.3 mg/mL at the study end, and in the active group the corresponding figures were 55.9 mg/mL and 58.0 mg/mL. A significantly smaller increase was demonstrated through repeated measurements of the two biomarkers in those on active supplementation. Active supplementation showed an effect on the CRP and sP-selectin levels, irrespective of the biomarker levels. Reduced cardiovascular mortality was demonstrated in both those with high and low levels of CRP and sP-selectin in the active supplementation group.. CRP and sP-selectin showed significant changes reflecting effects on inflammation and atherosclerosis in those given selenium and coenzyme Q10 combined. A reduced cardiovascular mortality could be demonstrated in the active group, irrespective of biomarker level. This result should be regarded as hypothesis-generating, and it is hoped it will stimulate more research in the area.

Topics: Aged; Aged, 80 and over; Biomarkers; C-Reactive Protein; Cardiovascular Diseases; Dietary Supplements; Double-Blind Method; Early Intervention, Educational; Enzyme-Linked Immunosorbent Assay; Female; Humans; Immunoenzyme Techniques; Inflammation; Male; Oxidative Stress; P-Selectin; Prognosis; Prospective Studies; Selenium; Survival Rate; Ubiquinone

This 12-week randomized placebo controlled clinical trial investigated the effect of Coenzyme Q10 (CoQ10) on diabetic neuropathy, oxidative stress, blood glucose and lipid profile of patients with type 2 diabetes.. Diabetic patients with neuropathic signs (n = 70) were randomly assigned to CoQ10 (200 mg/d) or placebo for 12 weeks. Blood samples were collected for biochemical analysis and neuropathy tests before and after the trial.. There were no significant differences between the two groups in terms of mean fasting blood glucose, HbA1c and the lipid profile after the trial. The mean insulin sensitivity and total antioxidant capacity (TAC) concentration significantly increased in the Q10 group compared to the placebo after the trial (P < 0.05). C-reactive protein (hsCRP) significantly decreased in the intervention group compared to placebo after the trial (P < 0.05). In the control group, insulin sensitivity decreased and HOMA-IR increased, which revealed a significant difference between groups after the trial. Neuropathic symptoms and electromyography measurements did not differ between two groups after the trial.. According to the present study, CoQ10, when given at a dose of 200 mg/d for 12 weeks to a group of neuropathic diabetic patients, did not improve the neuropathy signs compared to placebo, although it had some beneficial effects on TAC and hsCRP and probably a protective effect on insulin resistance.

Topics: Blood Glucose; Diabetic Neuropathies; Double-Blind Method; Female; Humans; Inflammation; Male; Middle Aged; Oxidative Stress; Ubiquinone

High oxidative stress and chronic inflammation can contribute to the pathogenesis of coronary artery disease (CAD). Coenzyme Q10 is an endogenous lipid-soluble antioxidant. Statins therapy can reduce the biosynthesis of coenzyme Q10. The purpose of this study was to investigate the effects of a coenzyme Q10 supplement (300 mg/d; 150 mg/b.i.d) on antioxidation and anti-inflammation in patients who have CAD during statins therapy.. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery and who were treated with statins for at least one month were enrolled in this study. The subjects (n = 51) were randomly assigned to the placebo (n = 24) and coenzyme Q10 groups (Q10-300 group, n = 27). The intervention was administered for 12 weeks. The concentrations of coenzyme Q10, vitamin E, antioxidant enzymes activities (superoxide dismutase, catalase, and glutathione peroxidase), and inflammatory markers [C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6)] were measured in the 42 subjects (placebo, n = 19; Q10-300, n = 23) who completed the study.. The levels of the plasma coenzyme Q10 (P < 0.001) and antioxidant enzymes activities (P < 0.05) were significantly higher after coenzyme Q10 supplementation. The levels of inflammatory markers (TNF-α, P = 0.039) were significantly lower after coenzyme Q10 supplementation. The subjects in the Q10-300 group had significantly higher vitamin E (P = 0.043) and the antioxidant enzymes activities (P < 0.05) than the placebo group at week 12. The level of plasma coenzyme Q10 was significantly positively correlated with vitamin E (P = 0.008) and antioxidant enzymes activities (P < 0.05) and was negatively correlated with TNF-α (P = 0.034) and IL-6 (P = 0.027) after coenzyme Q10 supplementation.. Coenzyme Q10 supplementation at 300 mg/d significantly enhances antioxidant enzymes activities and lowers inflammation in patients who have CAD during statins therapy.. ClinicalTrials.gov Identifier: NCT01424761.

Topics: Aged; Aged, 80 and over; C-Reactive Protein; Catalase; Coronary Artery Disease; Dietary Supplements; Dose-Response Relationship, Drug; Female; Glutathione Peroxidase; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Inflammation; Interleukin-6; Male; Middle Aged; Oxidative Stress; Single-Blind Method; Superoxide Dismutase; Tumor Necrosis Factor-alpha; Ubiquinone

We have investigated whether the quality of dietary fat and supplementation with coenzyme Q(10) (CoQ) modifies expression of genes related with inflammatory response and endoplasmic reticulum stress in elderly persons. Twenty participants received three diets for 4 weeks each: Mediterranean diet + CoQ (Med + CoQ), Mediterranean diet (Med), and saturated fatty acid-rich diet (SFA). After 12-hour fast, volunteers consumed a breakfast with a fat composition similar to that consumed in each of the diets. Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet. Med + CoQ diet produced a lower postprandial decrease p65 and IKK-b gene expression compared with the other diets. Our results support the anti-inflammatory effect of Med diet and that exogenous CoQ supplementation in synergy with a Med diet modulates the inflammatory response and endoplasmic reticulum stress.

Topics: Aged; Body Mass Index; Calreticulin; Cross-Over Studies; Diet, Mediterranean; Dietary Fats; Dietary Supplements; DNA-Binding Proteins; Endoplasmic Reticulum Chaperone BiP; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation; Heat-Shock Proteins; Humans; I-kappa B Kinase; Inflammation; Interleukin-1beta; Leukocytes, Mononuclear; Male; Matrix Metalloproteinase 9; Mitogen-Activated Protein Kinase 8; Regulatory Factor X Transcription Factors; Transcription Factors; Ubiquinone

Mitochondrial dysfunction is associated with increased mortality in septic shock. Coenzyme Q10 (CoQ10) is a key cofactor in the mitochondrial respiratory chain, but whether CoQ10 is depleted in septic shock remains unknown. Moreover, statin therapy may decrease CoQ10 levels, but whether this occurs acutely remains unknown. We measured CoQ10 levels in septic shock patients enrolled in a randomized trial of simvastatin versus placebo.. We conducted a post hoc analysis of a prospective, randomized trial of simvastatin versus placebo in patients with septic shock (ClinicalTrials.gov ID: NCT00676897). Adult patients with suspected or confirmed infection and the need for vasopressor support were included in the initial trial. For the current analysis, blood specimens were analyzed for plasma CoQ10 and low-density lipoprotein (LDL) levels. The relationship between CoQ10 levels and inflammatory and vascular endothelial biomarkers was assessed using either the Pearson or Spearman correlation coefficient.. We analyzed 28 samples from 14 patients. CoQ10 levels were low, with a median of 0.49 (interquartile range 0.26 to 0.62) compared to levels in healthy control patients (CoQ10 = 0.95 μmol/L ± 0.29; P < 0.0001). Statin therapy had no effect on plasma CoQ10 levels over time (P = 0.13). There was a statistically significant relationship between plasma CoQ10 levels and levels of vascular cell adhesion molecule (VCAM) (r2 = 0.2; P = 0.008), TNF-α (r2 = 0.28; P = 0.004), IL-8 (r2 = 0.21; P = 0.015), IL-10 (r2 = 0.18; P = 0.025), E-selectin (r2 = 0.17; P = -0.03), IL-1ra (r2 = 0.21; P = 0.014), IL-6 (r2 = 0.17; P = 0.029) and IL-2 (r2 = 0.23; P = 0.009). After adjusting for LDL levels, there was a statistically significant inverse relationship between plasma CoQ10 levels and levels of VCAM (r2 = 0.24; P = 0.01) (Figure 3) and IL-10 (r2 = 0.24; P = 0.02).. CoQ10 levels are significantly lower in septic shock patients than in healthy controls. CoQ10 is negatively associated with vascular endothelial markers and inflammatory molecules, though this association diminishes after adjusting for LDL levels.

Topics: Cholesterol, LDL; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Inflammation; Male; Middle Aged; Prospective Studies; Shock, Septic; Ubiquinone; Vascular Cell Adhesion Molecule-1; Vitamins

Topics: Adult; C-Reactive Protein; Cross-Sectional Studies; Dietary Supplements; East Asian People; Humans; Inflammation; Male; Middle Aged; Vitamins

Vincristine is a chemotherapy drug that belongs to the vinca alkaloids group. It is used for treatment of hematologic malignancies and several solid tumors. Vincristine-induced peripheral neuropathy is a major dose-limiting side effect. Coenzyme Q10 (Co Q10), an essential component of the mitochondrial electron transport chain, participates in energy production. It is a powerful fat-soluble antioxidant and also exerts anti-inflammatory effects. Therefore, this study was aimed to focus on the mechanistic insights of vincristine-induced peripheral neuropathy in addition to shedding the light on the modulatory effect of Co Q10. Twenty-eight rats were randomly divided into four groups. Peripheral neuropathy was induced by intraperitoneal injection of vincristine (0.1 mg/kg body weight). Co Q10 was injected intraperitoneally (10 mg/kg body weight) for 24 days. Sciatic nerve MDA, TAC, GSH, 8-OHdG, TNF-α, IL-1β, and NF-κB levels were assessed. Gene expression of SARM1 and Nrf2 was also assessed. Serum neurofilament light chain was immunoassayed, in addition to the behavioral assessment. Co Q10 significantly improved oxidative stress and inflammatory biomarkers. It also decreased serum NFL levels. It enhanced Nrf2 and decreased SARM1 gene expression. Histopathological findings proved the biochemical and molecular findings. Our results support Co Q10 as a potential protective agent against vincristine-induced peripheral neuropathy.

Topics: Animals; Inflammation; Oxidative Stress; Peripheral Nervous System Diseases; Rats; Rats, Sprague-Dawley; Ubiquinone; Vincristine

Niemann Pick type C is an inborn error of metabolism (IEM), classified as a lysosomal storage disease (LSD) caused by a dysfunction in NPC transport protein, that leads to intracellular accumulation of non-esterified cholesterol and other lipids. Clinical manifestations are ample, with visceral and neurological symptoms. Miglustat, a molecule that reversibly inhibits glucosylceramide synthase is used as treatment for this disorder. Studies demonstrated the influence of oxidative stress and inflammation in IEM, as well in animal model of NP-C disease. Nonetheless, literature lacks data on patients, so our work aimed to investigate if there is influence of chronic inflammation in the pathophysiology of NP-C disease, and the effect of miglustat, N-acetylcysteine (NAC) and Coenzyme Q10 (CoQ10). We evaluated the plasmatic cytokines in NPC patients at diagnosis and during the treatment with miglustat. Additionally, we performed an in vitro study with antioxidants NAC (1 mM and 2.5 mM) and CoQ10 (5 μM and 10 μM), where we could verify its effect on inflammatory parameters, as well as in cholesterol accumulation. Our results showed that NP-C patients have higher plasmatic levels of pro and anti-inflammatory cytokines (IL-6, IL-8, and IL-10) at diagnosis and the treatment with miglustat was able to restore it. In vitro study showed that treatment with antioxidants in higher concentrations significantly decrease cholesterol accumulation, and NAC at 2.5 mM normalized the level of pro-inflammatory cytokines. Although the mechanism is not completely clear, it can be related to restoration in lipid traffic and decrease in oxidative stress caused by antioxidants.

Topics: 1-Deoxynojirimycin; Acetylcysteine; Antioxidants; Cholesterol; Cytokines; Enzyme Inhibitors; Humans; Inflammation; Niemann-Pick Disease, Type C; Ubiquinone

Osteoarthritis (OA) is the most common degenerative joint disease and is characterized by breakdown of joint cartilage. Coenzyme Q10 (CoQ10) exerts diverse biological effects on bone and cartilage; observational studies have suggested that CoQ10 may slow OA progression and inflammation. However, any effect of CoQ10 on OA remains unclear. Here, we investigated the therapeutic utility of CoQ10-micelles.. Seven-week-old male Wistar rats were injected with monosodium iodoacetate (MIA) to induce OA. CoQ10-micelles were administered orally to MIA-induced OA rats; celecoxib served as the positive control. Pain, tissue destruction, and inflammation were measured. The expression levels of catabolic and inflammatory cell death markers were assayed in CoQ10-micelle-treated chondrocytes.. Oral supplementation with CoQ10-micelles attenuated OA symptoms remarkably, including pain, tissue destruction, and inflammation. The expression levels of the inflammatory cytokines IL-1β, IL-6, and MMP-13, and of the inflammatory cell death markers RIP1, RIP3, and pMLKL in synovial tissues were significantly reduced by CoQ10-micelle supplementation, suggesting that CoQ10-micelles might attenuate the synovitis of OA. CoQ10-micelle addition to cultured OA chondrocytes reduced the expression levels of catabolic and inflammatory cell death markers.. CoQ10-micelles might usefully treat OA.

Topics: Animals; Cartilage, Articular; Cell Death; Chondrocytes; Disease Models, Animal; Inflammation; Iodoacetic Acid; Male; Micelles; Nociceptive Pain; Osteoarthritis; Rats; Rats, Wistar; Ubiquinone

Propionic acid (PPA) is a short-chain fatty acid produced endogenously by gut microbiota and found in foodstuffs and pharmaceutical products as an additive. Exposure to PPA has been associated with the development of autism spectrum disorder (ASD). The purpose of this study was to investigate the protective effect of acetyl-L-carnitine (ALCAR) and liposomal Co-enzyme Q10 (CoQ10) against cerebral and cerebellar oxidative injury, inflammation, and cell death, and alterations in ALDH1A1-RA-RARα signaling in an autism-like rat model induced by PPA. The rats were treated with PPA and concurrently received ALCAR and/or CoQ10 for 5 days. The animals were sacrificed, and the cerebral cortex and cerebellum were collected for analysis. PPA caused histopathological alterations along with increased malondialdehyde (MDA), NF-κB p65, TNF-α, and IL-6 in the cerebrum and cerebellum of rats. Reduced glutathione (GSH) and antioxidant enzymes were declined in the brain of rats that received PPA. Concurrent treatment with ALCAR and/or CoQ10 prevented tissue injury, decreased MDA, NF-κB p65, and pro-inflammatory cytokines, and enhanced cellular antioxidants in PPA-administered rats. ALCAR and/or CoQ10 upregulated Bcl-2 and decreased Bax and caspase-3 in the brain of rats. In addition, ALCAR and/or CoQ10 upregulated cerebral and cerebellar ALDH1A1 and RARα in PPA-treated rats. The combination of ALCAR and CoQ10 showed more potent effects when compared with the individual treatments. In conclusion, ALCAR and/or CoQ10 prevented tissue injury, ameliorated oxidative stress, inflammatory response, and apoptosis, and upregulated ALDH1A1-RA-RARα signaling in the brain of autistic rats.

Topics: Acetylcarnitine; Animals; Antioxidants; Autism Spectrum Disorder; Inflammation; Neurotoxicity Syndromes; NF-kappa B; Oxidative Stress; Propionates; Rats; Ubiquinone

The present study aimed to investigate the rationale and efficacy of using a citicoline, coenzyme Q10 (CAVAQ10) and vitamin B3 fixed combination in combating inflammation and oxidation in neuronal cells exposed to oxidative stress.. HypoE22 cells and isolated hypothalamic specimens were selected as in vitro models to conduct the experiments. The efficacy of citicoline, CAVAQ10, and vitamin B3, with their fixed combination, were assayed after the exposure of hypothalamic cells to hydrogen peroxide (concentration range 1 nM-10 µM), in order to evaluate the biocompatibility of treatments. The activity of neuroprotective and pro-inflammatory factors, namely, brain-derived neurotrophic factor (BDNF), interleukin-6 (IL-6), and tumor necrosis factor-α (TNFα), involved in the neuronal cell damage in neurodegenerative diseases, were assayed in isolated hypothalamus.. Neither citicoline, CAVAQ10, nor vitamin B3 significantly altered hypothalamic cell viability, thus suggesting the biocompatibility of single ingredients and fixed combination in the concentration range considered for the study. In the same condition, citicoline and CAVAQ10 were also effective in reducing the gene expression of monoaminoxidase-B, involved in dopamine degradation. However, only citicoline demonstrated an ability to reduce dopamine levels. Conversely, all compounds were effective in reducing the gene expression of IL-6, and TNFα, and in inducing the gene expression of BDNF, with the co-administration of citicoline/CAVAQ10/vitamin B3 being generally more effective than single ingredients.. The present findings support the beneficial and synergistic effects of citicoline, CAVAQ10, and vitamin B3 in fixed combination in reducing inflammation and oxidation, and in stimulating neurotrophin production in neuronal cells.

Topics: Brain-Derived Neurotrophic Factor; Cytidine Diphosphate Choline; Dopamine; Humans; Inflammation; Interleukin-6; Niacinamide; Oxidative Stress; Tumor Necrosis Factor-alpha; Ubiquinone

Our work was aimed at investigating the impact and regulatory mechanism of coenzyme Q10 (. HS decreased the activity of the testicular antioxidant system, superoxide dismutase, glutathione peroxidase, and catalase, while the amount of lipid peroxidation (malondialdehyde) was increased. The index of apoptosis and mRNA expression of caspase 3 and Bax were increased, while the mRNA expression levels of Bcl-2, 3β-HSD, and 17β-HSD3 decreased after HS. Exposure to HS decreased the serum testosterone level but increased the activation of pro-inflammatory cytokines (interleukin 1 beta and tumor necrosis factor-alpha). Deleterious effects of HS on the mentioned parameters were reduced when the rats were treated with

Topics: Animals; Apoptosis; Glutathione Peroxidase; Heat-Shock Response; Inflammation; Lipid Peroxidation; Male; Malondialdehyde; Oxidative Stress; Rats; Superoxide Dismutase; Testis; Ubiquinone

Multiple Sclerosis (MS) is a chronic, progressive demyelinating disease of the central nervous system that causes the most disability in young people, besides trauma. Coenzyme Q10 (CoQ10)-also known as ubiquinone-is an endogenous lipid-soluble antioxidant in the mitochondrial oxidative respiratory chain which can reduce oxidative stress and inflammation, the processes associated with demyelination in MS. Cuprizone (CPZ) intoxication is a well-established model of inducing MS, best for studying demyelination-remyelination. In this study, we examined for the first time the role of CoQ10 in preventing demyelination and induction of remyelination in the chronic CPZ model of MS. 40 male mice were divided into four groups. 3 group chewed CPZ-containing food for 12 weeks to induce MS. After 4 weeks, one group were treated with CoQ10 (150 mg/kg/day) by daily gavage until the end of the experiment, while CPZ poisoning continued. At the end of 12 weeks, tail suspension test (TST) and open field test (OFT) was taken and animals were sacrificed to assess myelin basic protein (MBP), oligodendrocyte transcription factor-1 (Olig1), tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) by real-time polymerase chain reaction (real-time PCR) and total antioxidant capacity (TAC) and superoxide dismutase (SOD) by Elisa test. Luxol fast blue (LFB) staining was used to evaluate histological changes. CoQ10 administration promoted remyelination in histological findings. MBP and Olig-1 expression were increased significantly in CoQ10 treated group compare to the CPZ-intoxicated group. CoQ10 treatment alleviated stress oxidative status induced by CPZ and dramatically suppress inflammatory biomarkers. CPZ ingestion made no significant difference between normal control group and the CPZ-intoxicated group in TST and OFT. CoQ10 can enhance remyelination in the CPZ model and potentially might have same effects in MS patients.

Topics: Animals; Behavior, Animal; Biomarkers; Chronic Disease; Corpus Callosum; Cuprizone; Cytokines; Demyelinating Diseases; Disease Models, Animal; Inflammation; Inflammation Mediators; Mice, Inbred C57BL; Multiple Sclerosis; Myelin Sheath; Oxidative Stress; Remyelination; Ubiquinone

Radiation enteropathy is one the most common clinical issue for patients receiving radiotherapy for abdominal/pelvic tumors which severely affect the quality of life of cancer patients due to dysplastic lesions (ischemia, ulcer, or fibrosis) that aggravate the radiation damage. Herein, this study demonstrated the prophylactic role of coenzyme Q10 (CoQ10), a powerful antioxidant, against radiotherapy-induced gastrointestinal injury. Male Sprague Dawley rats were divided into four groups: group 1 was defined as control, and group 2 was the irradiated group. Group 3 and 4 were CoQ10 control and radiation plus CoQ10 groups, respectively. CoQ10 (10 mg/kg) was orally administered for 10 days before 10 Gy whole-body radiation and was continued for 4 days post-irradiation. CoQ10 administration protected rats delivered a lethal dose of ϒ-radiation from changes in crypt-villus structures and promoted regeneration of the intestinal epithelium. CoQ10 attenuated radiation-induced oxidative stress by decreasing lipid peroxidation and increasing the antioxidant enzyme catalase activity and reduced glutathione level. CoQ10 also counteracts inflammatory response mediated after radiation exposure through downregulating intestinal NF-ĸB expression which subsequently decreased the level of inflammatory cytokine IL-6 and the expression of COX-2. Radiation-induced intestinal fibrosis confirmed via Masson's trichrome staining occurred through upregulating transforming growth factor (TGF)-β1 and matrix metalloproteinase (MMP)-9 expression, while CoQ10 administration significantly diminishes these effects which further confirmed the anti-fibrotic property of CoQ10. Therefore, CoQ10 is a promising radioprotector that could prevent intestinal complications and enhance the therapeutic ratio of radiotherapy in patients with pelvic tumors through suppressing the NF-kB/TGF-β1/MMP-9 signaling pathway.

Topics: Animals; Disease Models, Animal; Fibrosis; Gene Expression Regulation; Inflammation; Intestinal Diseases; Male; Matrix Metalloproteinase 9; NF-kappa B; Radiation Injuries; Rats; Rats, Sprague-Dawley; Transforming Growth Factor beta; Ubiquinone; Vitamins

Topics: Administration, Oral; Animals; Humans; Inflammation; Malaria, Cerebral; Mice; Oxidative Stress; Ubiquinone

A role for mitochondrial dysfunction has been proposed in the immune dysregulation and organ damage characteristic of systemic lupus erythematosus (SLE). Idebenone is a coenzyme Q10 synthetic quinone analog and an antioxidant that has been used in humans to treat diverse diseases in which mitochondrial function is impaired. This study was undertaken to assess whether idebenone ameliorates lupus in murine models.. Idebenone was administered orally to MRL/lpr mice at 2 different doses (1 gm/kg or 1.5 gm/kg idebenone-containing diet) for 8 weeks. At peak disease activity, clinical, immunologic, and metabolic parameters were analyzed and compared to those in untreated mice (n = 10 per treatment group). Results were confirmed in the lupus-prone NZM2328 mouse model.. In MRL/lpr mice, idebenone-treated mice showed a significant reduction in mortality incidence (P < 0.01 versus untreated mice), and the treatment attenuated several disease features, including glomerular inflammation and fibrosis (each P < 0.05 versus untreated mice), and improved renal function in association with decreased renal expression of interleukin-17A (IL-17A) and mature IL-18. Levels of splenic proinflammatory cytokines and inflammasome-related genes were significantly decreased (at least P < 0.05 and some with higher significance) in mice treated with idebenone, while no obvious drug toxicity was observed. Idebenone inhibited neutrophil extracellular trap formation in neutrophils from lupus-prone mice (P < 0.05) and human patients with SLE. Idebenone also improved mitochondrial metabolism (30% increase in basal respiration and ATP production), reduced the extent of heart lipid peroxidation (by one-half that of untreated mice), and significantly improved endothelium-dependent vasorelaxation (P < 0.001). NZM2328 mice exposed to idebenone also displayed improvements in renal and systemic inflammation, reducing the kidney pathology score (P < 0.05), IgG/C3 deposition (P < 0.05), and the gene expression of interferon, proinflammatory, and inflammasome-related genes (at least P < 0.05 and some with higher significance).. Idebenone ameliorates murine lupus disease activity and the severity of organ damage, supporting the hypothesis that agents that modulate mitochondrial biologic processes may have a therapeutic role in human SLE.

Topics: Animals; Antioxidants; Disease Models, Animal; Extracellular Traps; Inflammation; Interleukin-17; Interleukin-18; Kidney; Lupus Erythematosus, Systemic; Mice; Mice, Inbred MRL lpr; Mitochondria; Ubiquinone

Sevoflurane may exert neurotoxic effects on the developing brain. Coenzyme Q10 (CoQ10) has been reported to reduce sevoflurane anesthesia‑induced cognitive deficiency in 6‑day‑old mice. However, its specific mechanisms remain unknown. Apolipoprotein E (ApoE) has been reported to lead to the initiation of neurodegeneration in patients with Alzheimer's disease (AD) and may serve an important role in anesthesia‑induced neurotoxicity. The present study aimed to reveal the role of ApoE in the pathogenesis of tau protein hyperphosphorylation and neuroinflammation enhancement caused by sevoflurane anesthesia, as well as the protective mechanism of CoQ10 in an anesthetic sevoflurane treatment model of primary mouse hippocampal neurons. For that purpose, the neurons were randomly assigned to the following groups: i) Control; ii) sevoflurane; iii) control+corn oil; iv) sevoflurane+corn oil; v) control+CoQ10; and vi) control+CoQ10. CoQ10 or corn oil alone was added to the medium on day 4 of neuron culture. The neurons in the sevoflurane group were treated with 21% O2, 5% CO2 and 4.1% sevoflurane for 4 h, whereas the control group only with 21% O2 and 5% CO2 on day 5. Samples were collected immediately after anesthesia or control treatment. ATP, superoxidase dismutase (SOD)1, ApoE mRNA, total ApoE, full‑length ApoE, ApoE fragments, Tau5, Tau‑PS202/PT205 (AT8), Tau‑PSer396/404 (PHF1), tumor necrosis factor (TNF)‑α, interleukin (IL)‑6 and IL‑1β levels were measured with ELISA, quantitative PCR, western blotting and immunocytochemistry. The results of the present study indicated that sevoflurane anesthesia significantly decreased the ATP and SOD levels, but increased ApoE mRNA, total ApoE protein, full‑length ApoE, ApoE fragments, phosphorylated tau (AT8 and PHF1) and neuroinflammatory factor (TNF‑α, IL‑6 and IL‑1β) expression levels compared with those in the control group. The use of CoQ10 reversed the expression of these factors. These results suggested that sevoflurane treatment damaged mouse hippocampal neurons, which may be associated with the expression of ApoE and its toxic fragments. CoQ10 improved energy replenishment and inhibited oxidative stress, which may lead to a decrease in ApoE and phosphorylated tau protein expression, thus mitigating the sevoflurane‑induced neuroinflammation in mouse hippocampal neurons.

Topics: Anesthetics, Inhalation; Animals; Apolipoproteins E; Cells, Cultured; Hippocampus; Inflammation; Mice; Mice, Inbred C57BL; Neurons; Neuroprotective Agents; Neurotoxicity Syndromes; Phosphorylation; Sevoflurane; tau Proteins; Ubiquinone

Neonatal ischemic stroke has a higher incidence than childhood stroke. Seizures are the first sign for the need for clinical assessment in neonates, but many questions remain regarding treatments and follow-up modalities. In the absence of a known pathophysiological mechanism, only supportive care is currently provided. Stroke-induced microglia activation and neuroinflammation are believed to play a central role in the pathological progression of neonatal ischemic stroke. We induced a photothrombotic infarction with Rose Bengal in neonatal rats to investigate the effects of pre- and post-treatment with Aspirin (ASA), Clopidogrel (Clop), and Coenzyme Q10 (CoQ10), which are known for their neuroprotective effects in adult stroke. Pre-stroke medication ameliorates cerebral ischemic injury and reduces infarct volume by reducing microglia activation, cellular reactive oxygen species (ROS) production, and cytokine release. Post-stroke administration of ASA, Clop, and CoQ10 increased motor function and reduced the volume of infarction, and the statistical evidence was stronger than that seen in the pre-stroke treatment. In this study, we demonstrated that ASA, Clop, and CoQ10 treatment before and after the stroke reduced the scope of stroke lesions and increased behavioral activity. It suggests that ASA, Clop, and CoQ10 medication could significantly have neuroprotective effects in the neonates who have suffered strokes.

Topics: Animals; Animals, Newborn; Aspirin; Brain Ischemia; Clopidogrel; Disease Models, Animal; Inflammation; Neuroprotective Agents; Rats; Rose Bengal; Stroke; Ubiquinone

Parkinson's disease is a neurodegenerative disorder, and no treatment has been yet established to prevent disease progression. Coenzyme Q10, an antioxidant, has been considered a promising neuroprotective agent; however, conventional oral administration provides limited efficacy due to its very low bioavailability. In this study, we hypothesised that continuous, intrastriatal administration of a low dose of Coenzyme Q10 could effectively prevent dopaminergic neuron degeneration. To this end, a Parkinson's disease rat model induced by 6-hydroxydopamine was established, and the treatment was applied a week before the full establishment of this disease model. Behavioural tests showed a dramatically decreased number of asymmetric rotations in the intrastriatal Coenzyme Q10 group compared with the no treatment group. Rats with intrastriatal Coenzyme Q10 exposure also exhibited a larger number of dopaminergic neurons, higher expression of neurogenetic and angiogenetic factors, and less inflammation, and the effects were more prominent than those of orally administered Coenzyme Q10, although the dose of intrastriatal Coenzyme Q10 was 17,000-times lower than that of orally-administered Coenzyme Q10. Therefore, continuous, intrastriatal delivery of Coenzyme Q10, especially when combined with implantable devices for convection-enhanced delivery or deep brain stimulation, can be an effective strategy to prevent neurodegeneration in Parkinson's disease.

Topics: Administration, Oral; Animals; Apomorphine; Corpus Striatum; Dopaminergic Neurons; Dose-Response Relationship, Drug; Down-Regulation; Inflammation; Infusion Pumps, Implantable; Infusions, Parenteral; Male; Neovascularization, Physiologic; Neurogenesis; Neuroprotective Agents; Oxidopamine; Parkinsonian Disorders; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha; Tyrosine 3-Monooxygenase; Ubiquinone

Coenzyme Q10 (CoQ10), also known as ubiquinone, is a fat-soluble antioxidant. Although CoQ10 has not been approved as medication by the Food and Drug Administration, it is widely used in dietary supplements. Some studies have shown that CoQ10 has anti-inflammatory effects on various autoimmune disorders. In this study, we investigated the anti-inflammatory effects of liposome/gold hybrid nanoparticles encoded with CoQ10 (LGNP-CoQ10). Both CoQ10 and LGNP-CoQ10 were administered orally to mice with collagen-induced arthritis (CIA) for 10 weeks. The inflammation pathology of joint tissues of CIA mice was then analyzed using hematoxylin and eosin and Safranin O staining, as well as immunohistochemistry analysis. We obtained immunofluorescence staining images of spleen tissues using confocal microscopy. We found that pro-inflammatory cytokines were significantly decreased in LGNP-CoQ10 injected mice. Th17 cell and phosphorylated STAT3-expressed cell populations were also decreased in LGNP-CoQ10 injected mice. When human peripheral blood mononuclear cells (PBMCs) were treated with CoQ10 and LGNP-CoQ10, the IL-17 expression of PBMCs in the LGNP-CoQ10-treated group was significantly reduced. Together, these results suggest that LGNP-CoQ10 has therapeutic potential for the treatment of rheumatoid arthritis.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Arthritis, Experimental; Arthritis, Rheumatoid; Autoimmune Diseases; Cell Line; Cytokines; Disease Models, Animal; Gold; Humans; Inflammation; Interleukin-17; Leukocytes, Mononuclear; Liposomes; Male; Metal Nanoparticles; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; STAT3 Transcription Factor; T-Lymphocytes, Regulatory; Th17 Cells; Ubiquinone

Polycystic ovary syndrome (PCOS) is one of the common gynecological endocrine system diseases. It is characterized by excessive androgen, rare or anovulation, and polycystic ovary morphology. Coenzyme Q10 (CoQ10) is a fat-soluble natural vitamin, which has a continuous oxidation-reduction cycle and is an effective antioxidant that can protect ovaries from oxidative damage. This study aims to systematically summarize and analyze the scientific literatures on glucose metabolism index, lipid profiles, inflammatory factor, and sex hormone level of PCOS patients treated with CoQ10 to provide a reference basis for clinical treatment.. We will retrieve the following electronic databases from the built-in until March 2021: Cochrane Library, PubMed, EMBASE, Web of Science, China National Knowledge Infrastructure (CNKI), Chinese Biomedical Literature Database (CBM), Clinical Trials. gov, Chinese Scientific Journal Database (VIP), and Wang-fang database. Two reviewers will independently scan the articles searched, de-duplication, filtering, quality assessment. Differences will be resolved by discussion between the 2 reviewers or by a third reviewers. All analyses were systematic to evaluate interventions based on the Cochrane handbook. Meta-analysis and/or subgroup analysis will be performed on the basis of the included studies.. This review will be to investigate the efficacy of CoQ10 supplementation on glucose metabolism, lipid profiles, and biomarkers of inflammation in women with PCOS and provide a high-quality synthesis to assess whether CoQ10 is an effective and safe intervention for PCOS. The results of the analysis will be published in a scientific journal after peer-review.. INPLASY 2020100013.

Topics: Biomarkers; Blood Glucose; Female; Humans; Inflammation; Lipids; Meta-Analysis as Topic; Polycystic Ovary Syndrome; Research Design; Systematic Reviews as Topic; Treatment Outcome; Ubiquinone; Vitamins

Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1

Topics: Alanine Transaminase; Animals; Autophagy; Beclin-1; Body Weight; Disease Models, Animal; Gene Expression Regulation; Immunohistochemistry; Inflammation; Interleukin-6; Liver; Liver Diseases; Male; Mice; Mice, Inbred BALB C; Pyroptosis; Sepsis; Tumor Necrosis Factor-alpha; Ubiquinone; Up-Regulation

Chronic intensive exercise and hyperthermia may cause immune system function disturbance. We aimed to investigate the effect of 14-day coenzyme Q

Topics: Administration, Oral; Adolescent; Adult; C-Reactive Protein; Cold Temperature; Cytokines; Dietary Supplements; Exercise; Humans; Inflammation; Inflammation Mediators; Interleukin-10; Interleukin-6; Interleukin-8; Male; Oxidative Stress; Swimming; Tumor Necrosis Factor-alpha; Ubiquinone; Young Adult

Topics: Animals; Inflammation; Mice; Mitochondria; Ubiquinone

Competent detrusor muscles with coordinated contraction and relaxation are crucial for normal urinary bladder storage and emptying functions. Hence, detrusor instability, and subsequently bladder overactivity, may lead to undesirable outcomes including incontinence. Multiple mechanisms may underlie the pathogenesis of detrusor overactivity including inflammation and oxidative stress. Herein, we tested the possibility that CoQ10 may have a potential therapeutic role in detrusor overactivity.. Forty adult male Wistar albino rats weighing 100-150 g were used in the present study. Rats were divided (10/group) into control (receiving vehicles), monosodium glutamate (MSG)-treated (receiving 5 mg/kg MSG daily for 15 consecutive days), MSG + OO-treated (receiving concomitantly 5 mg/kg MSG and olive oil for 15 consecutive days), MSG + CoQ10-treated (receiving concomitantly 5 mg/kg MSG and 100 mg/kg CoQ10 daily for 15 consecutive days) groups.. MSG resulted in significant increase in bladder weight and sensitised the bladder smooth muscles to acetylcholine. MSG has also resulted in significant increase in bladder TNF-α, IL-6, malondialdehyde, nerve growth factor and connexion 43, with significant decrease in the antioxidant enzymes superoxide dismutase and catalase. Olive oil had no effect on MSG induced alterations of different parameters. Treatment with CoQ10 has resulted in a significant restoration of all the altered parameters.. Taken together, our results suggest that CoQ10 antagonizes the deleterious effects of MSG on detrusor activity. We propose that CoQ10 could be a therapeutic strategy targeting urinary bladder dysfunction.

Topics: Animals; Gap Junctions; Inflammation; Male; Muscle, Smooth; Oxidative Stress; Rats; Rats, Wistar; Sodium Glutamate; Ubiquinone; Urinary Bladder; Urinary Bladder, Overactive

Bipolar disorder (BPD) is a severe and chronic mental disease with high rates of social and functional disability. To explain the emergence and maintenance of BPD, increasing attention has been focused on dimensions of inflammation and oxidative stress (OTS). Coenzyme Q10 (CoQ10) is known for its anti-oxidant and anti-inflammatory effects; accordingly, the aim of the present study was to investigate, if compared to placebo, adjuvant CoQ10 might favorably impact on serum levels of inflammatory and OTS biomarkers in patients with BPD during their depressive phase. A total of 89 BPD patients, currently in a depressive episode were allocated by block randomization either to the adjuvant CoQ10 (200 mg/day) condition or to the placebo condition. At baseline and 8 weeks later at the end of the study, serum levels of total antioxidant capacity (TAC), total thiol groups (TTG), catalase activity (CAT), nitric oxide (NO), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interlukin-6 (IL-6), and IL-10 were assessed. 69 patients completed the 8-week lasting study. Compared to baseline and to the placebo condition, serum levels of TTG and TAC significantly increased, and TNF-α, IL-10, and NO statistically decreased over time in the adjuvant CoQ10 condition. No statistically significant changes were observed for CAT, MDA, and IL-6. The pattern of results suggests that compared to placebo and over a time lapse of 8 weeks, adjuvant CoQ10 favorably impacted on OTS and inflammatory biomarkers in patients with BPD during the depressive episode. Thus, CoQ10 might be considered a safe and effective strategy for treatment of patients with BPD during their depressive phase.

Topics: Adult; Antioxidants; Biomarkers; Bipolar Disorder; Chemotherapy, Adjuvant; Depression; Dietary Supplements; Female; Humans; Inflammation; Male; Middle Aged; Oxidative Stress; Ubiquinone

Current anticonvulsant therapies are principally aimed at suppressing neuronal hyperexcitability to prevent or control the incidence of seizures. However, the role of oxidative stress processes in seizures led to the proposition that antioxidant compounds may be considered as promising candidates for limiting the progression of epilepsy. Accordingly, the aim of this study is to determine if coenzyme Q10 (CoQ10) and alpha-tocopherol (α-Toc) have a neuroprotective effect in rats against the observed oxidative stress and inflammation during seizures induced by pentylenetetrazole (PTZ) in rats, and to study their interactions with the conventional antiseizure drug phenytoin (PHT), either alone or in combination. Overall, the data revealed that α-Toc and CoQ10 supplementation can ameliorate PTZ-induced seizures and recommended that nuclear factor erythroid 2-related factor 2 (NRF2) and silencing information regulator 1 (Sirt1) signaling pathways may exemplify strategic molecular targets for seizure therapies. The results of the present study provide novel mechanistic insights regarding the protective effects of antioxidants and suggest an efficient therapeutic strategy to attenuate seizures. Additionally, concurrent supplementation of CoQ10 and α-Toc may be more effective than either antioxidant alone in decreasing inflammation and oxidative stress in both cortical and hippocampal tissues. Also, CoQ10 and α-Toc effectively reverse the PHT-mediated alterations in the brain antioxidant status when compared to PHT only.

Topics: alpha-Tocopherol; Animals; Anticonvulsants; Antioxidants; Brain; Inflammation; Male; Neurons; Neuroprotective Agents; NF-E2-Related Factor 2; Oxidative Stress; Pentylenetetrazole; Phenytoin; Rats, Wistar; Seizures; Signal Transduction; Sirtuin 1; Ubiquinone

Coenzyme Q10 (Co-Q10) is extraordinarily popular and has been used in abundant interventions as an antioxidant reagent that participates in numerous oxidation reactions. According to substantial evidence previously reported, interleukin-1β (IL-1β) is deemed to be one of the chief orchestrator molecules in the degeneration of intervertebral disc (IVD). However, it is unknown whether Co-Q10 is able to protect against IVD degeneration. In the current study, mouse-derived IVDs as well as primary human nucleus pulposus (NP) cells were isolated and cultured. NP cells were stimulated with IL-1β, with or without selective addition of Co-Q10 to investigate the therapeutic effect of Co-Q10 on IVD degeneration. Levels of IL-1β-induced inflammatory biomarkers including TNF-α, COX-2, IL-6 and iNOS were reduced by Co-Q10, which was possibly associated with inhibition of NF-κB signaling activation. Furthermore, Co-Q10 maintained the production of anabolic biomarkers in NP cells such as collagen 2, aggrecan and Sox-9 and altered the enhanced catabolism induced by IL-1β. Moreover, the therapeutic role of Co-Q10 in sustaining IVD tissue-enhanced anabolism is potentially dependent on activation of the Akt signaling pathway. In summary, Co-Q10 may potentially represent an available molecular target that may shed light on approaches to the prevention and treatment of IVD degeneration in the future.

Topics: Animals; Cells, Cultured; Humans; Inflammation; Interleukin-1beta; Intervertebral Disc Degeneration; Mice; NF-kappa B; Nucleus Pulposus; RAW 264.7 Cells; Signal Transduction; Ubiquinone

Inflammation plays critical roles in the pathogenic mechanisms of several neurodegenerative disorders including Alzheimer's disease (AD). Previous study revealed that CoQ10 augmented cellular antioxidant defense capacity, thereby protecting PC12 cells from oxidative neurotoxicity. However, the mechanism by which CoQ10 inhibits inflammation remains unknown. In this study, we aim to examine the effects of CoQ10 on Aβ

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Apoptosis; Cell Survival; Inflammation; Neuroprotective Agents; NF-kappa B; NF-KappaB Inhibitor alpha; PC12 Cells; Peptide Fragments; Rats; Signal Transduction; Ubiquinone

Coenzyme Q10 (CoQ10) is a naturally occurring, lipid-soluble antioxidant and an essential electron carrier in the mitochondrial respiratory chain. In sepsis, CoQ10 deficiency induced by mitochondrial failure can lead to hypoxia, hypoperfusion, oxidative organ damage and finally death. We aimed to investigate the effects of CoQ10 on survival, mesenteric artery blood flow (MABF), vascular reactivity, oxidative and inflammatory injuries in cecal ligation and puncture (CLP)-induced sepsis.. Wistar rats were divided into Sham, CLP, Sham+CoQ10, CLP+CoQ10 subgroups. CoQ10 (10mg/kg/day) or vehicle (olive oil; 1mL/kg/day) was intraperitoneally injected for 15days. At 16th day, Sham or CLP operation was performed. 20h after the operations, MABF and phenylephrine responses of isolated aortic rings were measured. Tissue samples were obtained for histopathological and biochemical evaluations. Furthermore, survival rates were monitored throughout 96h.. CoQ10 prevented mesenteric hypoperfusion and aortic dysfunction induced by CLP. Survival rate was %0 at 46th h in CLP group, but in CLP+CoQ10 group it was 37.5% at the end of 96h. CLP-induced elevations of serum AST, ALT, LDH, BUN, Cr and inflammatory cytokine (tumor necrosis factor-alpha, interleukin-1 beta and interleukin-6) levels were blocked by CoQ10. CoQ10 restored the increased liver, lung, spleen and kidney malondialdehyde levels and as well as reduced liver and spleen glutathione levels. The protective effects of CoQ10 on multiple organ damage were also observed histopathologically.. CoQ10 showed protective effects in sepsis due to its preservative effects on mesenteric perfusion, aortic function and also its anti-inflammatory and antioxidative effects.

Topics: Animals; Aorta; Cecum; Cytokines; Disease Models, Animal; Female; Inflammation; Ligation; Malondialdehyde; Mesenteric Ischemia; Protective Agents; Rats; Rats, Wistar; Renal Circulation; Sepsis; Survival Rate; Ubiquinone

This study aimed to investigate the feasibility of producing semisolid formulations based on nanocapsule suspensions containing the association of the coenzyme Q10 and vitamin E acetate by adding gellan gum (2%) to the suspensions. Furthermore, we studied their application as an alternative for the treatment of inflammation induced by ultraviolet B (UVB) radiation. For this, an animal model of injury induced by UVB-radiation was employed. All semisolids presented pH close to 5.5, drug content above 95% and mean diameter on the nanometric range, after redispersion in water. Besides, the semisolids presented non-Newtonian flow with pseudoplastic behavior and suitable spreadability factor values. The results also showed that the semisolid containing coenzyme Q10-loaded nanocapsules with higher vitamin E acetate concentration reduced in 73±8% the UVB radiation-induced ear edema. Moreover, all formulations tested were able to reduce inflammation parameters evaluated through MPO activity and histological procedure on injured tissue and the semisolids containing the nanoencapsulated coenzyme Q10 reduced oxidative parameters assessment through the non-protein thiols levels and lipid peroxidation. This way, the semisolids based on nanocapsules may be considered a promising approach for the treatment and prevention of skin inflammation diseases.

Topics: Acetylglucosaminidase; Administration, Cutaneous; Animals; Edema; Hydrogen-Ion Concentration; Inflammation; Leukocytes; Light; Lipid Peroxidation; Mice; Nanocapsules; Nanostructures; Oxidative Stress; Particle Size; Peroxidase; Polysaccharides; Polysaccharides, Bacterial; Radiation Injuries; Rheology; Skin; Sulfhydryl Compounds; Sunburn; Tocopherols; Ubiquinone; Ultraviolet Rays

Coenzyme Q10 (CoQ10) has a potential role in the prevention and treatment of heart failure through improved cellular bioenergetics. In addition, it has antioxidant, free radical scavenging, and vasodilatory effects that may be beneficial. Although critical illness in intensive care unit is associated with decreased circulating CoQ10 levels, the clinical significance of CoQ10 levels during acute phase in the patients of cardiovascular disease remains unclear. We enrolled 257 consecutive cardiovascular patients admitted to the coronary care unit (CCU). Serum CoQ10 levels were measured after an overnight fast within 24 h of admission. We examined the comparison of serum CoQ10 levels between survivors and in-hospital mortalities in patients with cardiovascular disease. Serum CoQ10 levels during the acute phase in patients admitted to the CCU had similar independent of the diagnosis. CoQ10 levels were significantly lower in patients with in-hospital mortalities than in survivors (0.43 ± 0.19 vs. 0.55 ± 0.35 mg/L, P = 0.04). In patients admitted to the CCU, CoQ10 levels were negatively associated with age and C-reactive protein levels, and positively associated with body mass index, total cholesterol, and high-density lipoprotein cholesterol levels. Low CoQ10 levels correlated with low diastolic blood pressure. Multivariate logistic regression analysis demonstrated that low CoQ10 levels were an independent predictor of in-hospital mortality. Low serum CoQ10 levels during acute phase are significantly associated with cardiovascular risk and in-hospital mortality in patients admitted to the CCU.

Topics: Aged; Aged, 80 and over; Aging; C-Reactive Protein; Cardiovascular Diseases; Coronary Care Units; Female; Hospital Mortality; Hospitalization; Humans; Inflammation; Japan; Lipoproteins, HDL; Logistic Models; Male; Malnutrition; Middle Aged; Multivariate Analysis; Risk Factors; ROC Curve; Ubiquinone

(1) Background: Hepatocellular carcinoma (HCC) is the second leading cause of cancer deaths worldwide, and surgical resection is the main treatment for HCC. To date, no published study has examined the status of coenzyme Q10 in patients with HCC after surgery. Thus, the purpose of this study was to investigate the correlations between the level of coenzyme Q10, oxidative stress, and inflammation in patients with HCC after surgery; (2) Methods: 71 primary HCC patients were recruited. Levels of coenzyme Q10, vitamin E, oxidative stress (malondialdehyde), antioxidant enzymes activity (superoxidase dismutase, catalase, and glutathione peroxidase), and inflammatory markers (high sensitivity C-reactive protein; tumor necrosis factor-α; and interleukin-6) were measured; (3) Results: Patients with HCC had a significantly lower levels of coenzyme Q10 (

Topics: Adult; Aged; Aged, 80 and over; Aspartate Aminotransferases; Blood Glucose; C-Reactive Protein; Carcinoma, Hepatocellular; Creatinine; Glutathione Peroxidase; Humans; Inflammation; Interleukin-6; Linear Models; Liver Neoplasms; Malondialdehyde; Middle Aged; Oxidative Stress; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Tumor Necrosis Factor-alpha; Ubiquinone; Vitamin E; Young Adult

Anti-oxidant coenzyme Q10 (Co-Q10) is commonly used in clinic. Recently, Co-Q10 was reported to antagonize TNF-α-induced inflammation and play a protective role in various inflammatory conditions. However, its role in dermatitis is unknown. Herein, RAW264.7 macrophage cell line was cultured with stimulation of TNF-α, and administration of Co-Q10 alleviated TNF-α-mediated inflammatory reaction in vitro. Furthermore, oxazolone-induced dermatitis mice model was established, and treatment of Co-Q10 markedly attenuated dermatitis phenotype in this mice model. Moreover, the protective role of Co-Q10 in vitro and in dermatitis was probably due to its repression on NF-κB signaling. Collectively, Co-Q10 may represent a potential molecular target for prevention and treatment of inflammatory skin diseases.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Cell Line; Dermatitis, Contact; Disease Models, Animal; Inflammation; Interleukin-1beta; Interleukin-6; Macrophages; Male; Mice; Mice, Inbred C57BL; NF-kappa B; Oxazolone; Skin; Tumor Necrosis Factor-alpha; Ubiquinone

Topics: Alzheimer Disease; Anti-Inflammatory Agents, Non-Steroidal; Berberine; Humans; Inflammation; Metabolic Diseases; Selenium; Small Molecule Libraries; Ubiquinone; Vanadium Compounds

In the present study the relationship between the CoQ10 redox state (% oxidized form of CoQ10 ) and the serum level of c-reactive protein (CRP) was investigated in a large Caucasian study population (n = 1319). In order to evaluate independently the influence of the variables that predict the outcome of CRP, an analysis of covariance (ANCOVA) was performed with CRP as the dependent variable. Gender was taken as an independent factor and CoQ10 redox and BMI as independent covariates. Results were substantiated with findings from a human intervention study (n = 53), receiving 150 mg/day ubiquinol for 14 days. Spearman's correlation revealed a significant (P < 0.001) association between the CoQ10 redox state and CRP concentrations in the whole study population. Thus, higher CRP concentrations were found in subjects having more oxidized CoQ10 . Similar results were evident for further inflammatory markers (interleukin-6, number of leucocytes). The ANCOVA revealed a significant (P < 0.001) prediction of CRP concentrations by CoQ10 redox state, after controlling for the effect of BMI and separately for gender. In the intervention study it was further found that the oral intake of ubiquinol increased its proportion significantly (P < 0.001), with the highest increase in those persons having a low basal serum ubiquinol content (<92.3%). Here it was discovered that the ubiquinol status significantly correlated to the concentration of the inflammation marker monocyte chemotactic protein 1. It is concluded that CoQ10 redox state predicts the concentration of CRP. Persons at risk with lower ubiquinol status, higher BMI, and low grade inflammation may benefit from ubiquinol supplementation. © 2016 BioFactors, 42(3):268-276, 2016.

Topics: Adolescent; Adult; Body Mass Index; C-Reactive Protein; Chemokine CCL2; Dietary Supplements; Humans; Inflammation; Interleukin-6; Leukocyte Count; Male; Middle Aged; Oxidation-Reduction; Statistics, Nonparametric; Ubiquinone

Cisplatin (CP), a platinum based anticancer drug is used as one of the first-line therapy for the treatment of different types of solid tumors. However, CP-induced side effects particularly, nephrotoxicity is a major concern. A single nephrotoxic dose (7 mg/kg body weight) of CP was administered in rats with or without, pre and post combined multidoses of epigallocatechin gallate (EGCG) and coenzyme Q10 (CoQ10) (15 and 5 mg/kg body weight respectively). CP administration resulted in marked increase in the nephrotoxic parameters with alterations in the oxidative and nitrosative stress markers. The concentration of inflammatory, as well as apoptotic markers were markedly up-regulated in the kidney of the CP-treated group. Furthermore, CP resulted in histological injury in the renal tissues. Combined antioxidant treatment significantly (p < 0.01) attenuated CP-induced oxidative stress, nitrosative stress, inflammatory and apoptotic parameters. Moreover, an improvement in the histopathological changes confirmed the nephroprotective effect of antioxidant treatment. In conclusion, our study indicates that the combinatorial multidoses of EGCG and CoQ10 ameliorate the cisplatin-mediated pathogenesis by improving renal oxidative/nitrosative status, inflammation and apoptosis and thus can be used as a promising protective agent to increase the efficacy of the drug by minimizing its major side effect i.e. nephrotoxicity.

Topics: Animals; Antineoplastic Agents; Apoptosis; Catechin; Cisplatin; Inflammation; Kidney; Male; Nitrosation; Oxidative Stress; Rats; Rats, Wistar; Ubiquinone

Gout is a type of arthritis, which could result from the deposition of monosodium urate crystals in joints. It can cause redness, burning pain, inflammation of joints especially in big toe. In this study, we have looked for anti-arthritic effect of coenzyme Q10 (CoQ10) on monosodium urate crystal-induced inflammation in rats and compared it with that of the non-steroidal anti-inflammatory drug, indomethacin. The evaluation was done by measuring the paw volume, antioxidant status, lipid peroxidation, lysosomal enzymes (β-glcuronidase, β-galactosidase, N-acetyl-β-d-glucosaminidase, acid phosphatase) activities and histopathological studies. Paw volume, the levels of lysosomal enzymes, lipid peroxidation were significantly (P<0.05) increased and the antioxidant activity status was in turn decreased in monosodium urate crystal-induced rats. CoQ10 (10mg/kg/b.w. orally) treated monosodium urate crystal-induced rats showed near normal activities of lysosomal enzymes, reduced levels of lipid peroxidation, near normal paw volume and antioxidant status. CoQ10 was also able to minimize mononuclear cell infiltration and damage to articular cartilage. Current study indicates that CoQ10 possesses anti-inflammatory effect against gouty arthritis and can be used to treat acute form of gouty arthritis.

Topics: Animals; Anti-Inflammatory Agents; Arthritis, Gouty; Edema; Female; Inflammation; Lipid Peroxidation; Lysosomes; Rats; Rats, Wistar; Ubiquinone; Uric Acid

Low birth weight and rapid postnatal growth increases the risk of developing insulin resistance and type 2 diabetes in later life. However, underlying mechanisms and potential intervention strategies are poorly defined. Here we demonstrate that male Wistar rats exposed to a low-protein diet in utero that had a low birth weight but then underwent postnatal catch-up growth (recuperated offspring) had reductions in the insulin signaling proteins p110-β (13% ± 6% of controls [P < .001]) and insulin receptor substrate-1 (39% ± 10% of controls [P < .05]) in adipose tissue. These changes were not accompanied by any change in expression of the corresponding mRNAs, suggesting posttranscriptional regulation. Recuperated animals displayed evidence of a proinflammatory phenotype of their adipose tissue with increased IL-6 (139% ± 8% [P < .05]) and IL1-β (154% ± 16% [P < .05]) that may contribute to the insulin signaling protein dysregulation. Postweaning dietary supplementation of recuperated animals with coenzyme Q (CoQ10) (1 mg/kg of body weight per day) prevented the programmed reduction in insulin receptor substrate-1 and p110-β and the programmed increased in IL-6. These findings suggest that postweaning CoQ10 supplementation has antiinflammatory properties and can prevent programmed changes in insulin-signaling protein expression. We conclude that CoQ10 supplementation represents an attractive intervention strategy to prevent the development of insulin resistance that results from suboptimal in utero nutrition.

Topics: Adipose Tissue; Animals; Female; Gene Expression Profiling; Growth Disorders; Inflammation; Insulin; Insulin Resistance; Lipids; Male; Maternal Exposure; Maternal Nutritional Physiological Phenomena; Mice; MicroRNAs; Oxidative Stress; Phenotype; Rats; Rats, Wistar; Signal Transduction; Ubiquinone

Major long-term complications in patients with diabetes are related to oxidative stress, caused by the hyperglycaemia characteristic for diabetes mellitus. The anti-oxidant coenzyme Q10 (CoQ10) has therefore been proposed as a beneficial supplement to diabetes treatment. Apart from its anti-oxidative function, CoQ10 appears to modulate immune functions by largely unknown mechanisms. The aim of this study was therefore to investigate the effect of CoQ10 on antimicrobial peptides and natural killer (NK) cells, both innate immune components implicated in the pathogenesis of diabetes and diabetes-associated long-term complications such as cardiovascular disease. We determined serum levels of antimicrobial peptides and the phenotype of NK cells isolated from peripheral blood of patients with type 1 (T1DM) or type 2 diabetes mellitus (T2DM) and from healthy controls. In addition, the same parameters were determined in diabetic patients after a 12-week period of CoQ10 supplementation. Two antimicrobial peptides, the human cathelicidin antimicrobial peptide (CAMP) and the human beta defensin 1 (hBD1), were reduced in serum from patients with T1DM. This defect was not reversible by CoQ10 supplementation. In contrast, CoQ10 reduced the levels of circulating hBD2 in these patients and induced changes in subset distribution and activation markers in peripheral NK cells. The results of the present study open up novel approaches in the prevention of long-term complications associated to T1DM, although further investigations are needed.

Topics: Adult; Aged; Antimicrobial Cationic Peptides; Antioxidants; beta-Defensins; Biomarkers; Case-Control Studies; Cytokines; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Dietary Supplements; Humans; Immunity, Innate; Inflammation; Killer Cells, Natural; Middle Aged; Oxidative Stress; Ubiquinone

To investigate the effect of CoenzymeQ10 (CoQ10) on pain severity and cartilage degeneration in an experimental model of rat osteoarthritis (OA).. OA was induced in rats by intra-articular injection of monosodium iodoacetate (MIA) to the knee. Oral administration of CoQ10 was initiated on day 4 after MIA injection. Pain severity was assessed by measuring secondary tactile allodynia using the von Frey assessment test. The degree of cartilage degradation was determined by measuring cartilage thickness and the amount of proteoglycan. The mankin scoring system was also used. Expressions of matrix metalloproteinase-13 (MMP-13), interleukin-1β (IL-1β), IL-6, IL-15, inducible nitric oxide synthase (iNOS), nitrotyrosine and receptor for advanced glycation end products (RAGE) were analyzed using immunohistochemistry.. Treatment with CoQ10 demonstrated an antinociceptive effect in the OA animal model. The reduction in secondary tactile allodynia was shown by an increased pain withdrawal latency and pain withdrawal threshold. CoQ10 also attenuated cartilage degeneration in the osteoarthritic joints. MMP-13, IL-1β, IL-6, IL-15, iNOS, nitrotyrosine and RAGE expressions were upregulated in OA joints and significantly reduced with CoQ10 treatment.. CoQ10 exerts a therapeutic effect on OA via pain suppression and cartilage degeneration by inhibiting inflammatory mediators, which play a vital role in OA pathogenesis.

Topics: Analgesics; Animals; Cartilage; Cytokines; Disease Models, Animal; Gene Expression Regulation; Inflammation; Iodoacetic Acid; Male; Matrix Metalloproteinase 13; Nitric Oxide; Nitric Oxide Synthase Type II; Osteoarthritis; Pain; Rats; Rats, Wistar; Receptor for Advanced Glycation End Products; Receptors, Immunologic; Ubiquinone

Fibromyalgia (FM) is a complex disorder that affects up to 5% of the general population worldwide. Both mitochondrial dysfunction and inflammation have been implicated in the pathophysiology of FM. We have investigated the possible relationship between mitochondrial dysfunction, oxidative stress, and inflammation in FM. We studied 30 women diagnosed with FM and 20 healthy women. Blood mononuclear cells (BMCs) from FM patients showed reduced level of coenzyme Q₁₀ (CoQ₁₀) and mtDNA contents and high level of mitochondrial reactive oxygen species (ROS) and serum tumor necrosis factor (TNF)-alpha and transcript levels. A significant negative correlation between CoQ₁₀ and TNF-alpha levels (r=-0.588; p<0.01), and a positive correlation between ROS and TNF-alpha levels (r=0.791; p<0.001) were observed accompanied by a significant correlation of visual analogical scale with serum TNF-alpha and transcript levels (r=0.4507; p<0.05 and r=0.7089; p<0.001, respectively). TNF-alpha release was observed in an in vitro (BMCs) and in vivo (mice) CoQ₁₀ deficiency model. Oral CoQ₁₀ supplementation restored biochemical parameters and induced a significant improvement in clinical symptoms (p<0.001). These results lead to the hypothesis that inflammation could be a mitochondrial dysfunction-dependent event implicated in the pathophysiology of FM in several patients indicating at mitochondria as a possible new therapeutic target.

Topics: Animals; Disease Models, Animal; Female; Fibromyalgia; Humans; Inflammation; Leukocytes, Mononuclear; Male; Mice; Mitochondria; Reactive Oxygen Species; Tumor Necrosis Factor-alpha; Ubiquinone

Exhausting exercise induces muscle damage associated with high production of free radicals and pro-inflammatory mediators.. The objective of this study was to determine for the first time and simultaneously whether oral coenzyme Q(10) (CoQ(10)) supplementation can prevent over-expression of inflammatory mediators and oxidative stress associated with strenuous exercise.. The participants were classified in two groups: CoQ(10) group (CG) and placebo group (PG). The physical test consisted in a constant run (50 km) that combined several degrees of high effort (mountain run and ultra-endurance), in permanent climbing.. Exercise was associated with an increase in TNF-α, IL-6, 8-hydroxy-2'-deoxyguanosine (8-OHdG), and isoprostane levels, revealing the degree of inflammation and oxidative stress induced. Oral supplementation of CoQ(10) during exercise was efficient reducing oxidative stress (decreased membrane hydroperoxides, 8-OHdG and isoprostanes generation, increased catalase, and total antioxidant status), which would lead to the maintenance of the cell integrity. Data obtained also indicate that CoQ(10) prevents over-expression of TNF-α after exercise, together with an increase in sTNF-RII that limits the pro-inflammatory actions of TNF. Moreover, CoQ(10) supplementation reduced creatinine production.. CoQ(10) supplementation before strenuous exercise decreases the oxidative stress and modulates the inflammatory signaling, reducing the subsequent muscle damage.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Administration, Oral; Adult; Antioxidants; Athletes; Catalase; Deoxyguanosine; Dietary Supplements; Humans; Inflammation; Inflammation Mediators; Interleukin-6; Isoprostanes; Male; Oxidative Stress; Running; Signal Transduction; Tumor Necrosis Factor-alpha; Ubiquinone

The exact mechanisms underlying the role of oxidative stress in the pathogenesis and the prothrombotic or proinflammatory status of antiphospholipid syndrome (APS) remain unknown. Here, we investigate the role of oxidative stress and mitochondrial dysfunction in the proatherothrombotic status of APS patients induced by IgG-antiphospholipid antibodies and the beneficial effects of supplementing cells with coenzyme Q(10) (CoQ(10)). A significant increase in relevant prothrombotic and inflammatory parameters in 43 APS patients was found compared with 38 healthy donors. Increased peroxide production, nuclear abundance of Nrf2, antioxidant enzymatic activity, decreased intracellular glutathione, and altered mitochondrial membrane potential were found in monocytes and neutrophils from APS patients. Accelerated atherosclerosis in APS patients was found associated with their inflammatory or oxidative status. CoQ(10) preincubation of healthy monocytes before IgG-antiphospholipid antibody treatment decreased oxidative stress, the percentage of cells with altered mitochondrial membrane potential, and the induced expression of tissue factor, VEGF, and Flt1. In addition, CoQ(10) significantly improved the ultrastructural preservation of mitochondria and prevented IgG-APS-induced fission mediated by Drp-1 and Fis-1 proteins. In conclusion, the oxidative perturbation in APS patient leukocytes, which is directly related to an inflammatory and pro-atherothrombotic status, relies on alterations in mitochondrial dynamics and metabolism that may be prevented, reverted, or both by treatment with CoQ(10).

Topics: Adult; Antibodies, Antiphospholipid; Antiphospholipid Syndrome; Biomarkers; Case-Control Studies; Female; Humans; Immunoglobulin G; Inflammation; Male; Middle Aged; Mitochondria; Monocytes; Oxidative Stress; Peroxides; Thrombosis; Ubiquinone

The present investigation consists in the development and characterization of CoQ10 loaded PLGA nanoparticles (CoQ10-NPs, size < 100 nm) by a scalable emulsion-diffusion-evaporation method. Thermal and crystallinity analysis collectively corroborated that CoQ10 was entrapped into the NPs in amorphous form. The lyophilized CoQ10-NPs were found to be stable for a period of 6 months (at room temperature). In vitro cell culture studies indicated that CoQ10-NPs significantly quenched ROS with nearly 10 fold higher efficacy than free CoQ10. Further, positively charged CoQ10-NPs were localized in two major sources of ROS generation: mitochondria and lysosomes. CoQ10-NPs showed improved oral bioavailability (4.28 times) as compared to free CoQ10. Finally remarkably higher hepatoprotective and anti-inflammatory activity of CoQ10-NPs as compared to free CoQ10 was observed due to mitigation of deleterious effects associated with the generation of free radicals. As elucidated by live noninvasive animal imaging, the higher anti-inflammatory activity of CoQ10-NPs can be attributed to significant accumulation of these NPs in the inflamed tissues.

Topics: Animals; Biological Availability; Cell Line; Female; Freeze Drying; Humans; Inflammation; Materials Testing; Mice; Nanoparticles; Particle Size; Polymers; Random Allocation; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Thiobarbituric Acid Reactive Substances; Ubiquinone; X-Ray Diffraction

Diabetes and obesity are metabolic disorders induced by an excessive dietary intake of fat, usually related to inflammation and oxidative stress.. The aim of the study is to investigate the effect of the antioxidant coenzyme Q10 (CoQ10) on hepatic metabolic and inflammatory disorders associated with diet-induced obesity and glucose intolerance.. C57bl6/j mice were fed for 8 weeks, either a control diet (CT) or a high-fat diet plus 21% fructose in the drinking water (HFF). CoQ10 supplementation was performed in this later condition (HFFQ).. HFF mice exhibit increased energy consumption, fat mass development, fasting glycaemia and insulinemia and impaired glucose tolerance. HFF treatment promoted the expression of genes involved in reactive oxygen species production (NADPH oxidase), inflammation (CRP, STAMP2) and metabolism (CPT1alpha) in the liver. CoQ10 supplementation decreased the global hepatic mRNA expression of inflammatory and metabolic stresses markers without changing obesity and tissue lipid peroxides compared to HFF mice. HFF diets paradoxically decreased TBARS (reflecting lipid peroxides) levels in liver, muscle and adipose tissue versus CT group, an effect related to vitamin E content of the diet.. In conclusion, HFF model promotes glucose intolerance and obesity by a mechanism independent on the level of tissue peroxides. CoQ10 tends to decrease hepatic stress gene expression, independently of any modulation of lipid peroxidation, which is classically considered as its most relevant effect.

Topics: Animals; Biomarkers; Body Weight; Dietary Fats; Energy Metabolism; Fructose; Glucose; Glucose Intolerance; Homeostasis; Inflammation; Lipid Peroxides; Liver; Male; Mice; Mice, Inbred C57BL; Obesity; Oxidative Stress; Reactive Oxygen Species; RNA, Messenger; Ubiquinone

This work aimed to assess some pharmacological activities of coenzyme Q(10) (CoQ(10)) in animal experimental models.. The chick chorioallantoic membrane assay was used to evaluate anti-angiogenic activity of CoQ(10). Anti-inflammatory activity of CoQ(10) was confirmed using two animal models of inflammation. These were the vascular permeability and air pouch models, models of acute and sub-acute inflammation, respectively. Antinociceptive activity was assessed by the acetic acid-induced abdominal constriction response.. CoQ(10) dose-dependently displayed inhibition of chick chorioallantoic membrane angiogenesis. In the acetic acid-induced vascular permeability model in mice, CoQ(10) at 50, 100 and 200 mg/kg reduced vascular permeability from 0.74 +/- 0.01 (A(590)) to 0.67 +/- 0.01 (P < 0.01), 0.46 +/- 0.02 (P < 0.01) and 0.30 +/- 0.01 (P < 0.01), respectively. In the carrageenan-induced inflammation in the air pouch, CoQ(10) was able to diminish exudate volume, the number of polymorphonulcear leucocytes and nitrite content in the air pouches. CoQ(10) at 25, 50 and 100 mg/kg significantly reduced acetic acid-induced abdominal constriction in mice from 27.0 +/- 2.00 (number of abdominal constrictions) to 17.7 +/- 0.33 (P < 0.01), 9.3 +/- 0.67 (P < 0.01) and 1.3 +/- 0.33 (P < 0.01), respectively, suggesting a strong antinociceptive activity.. CoQ(10) possessed considerable anti-angiogenic, anti-inflammatory and antinociceptive activity, possibly via down-regulating the level of nitric oxide, which partly supported its use as a dietary supplement and in combination therapy.

Topics: Abdominal Pain; Analgesics; Angiogenesis Inhibitors; Animals; Anti-Inflammatory Agents; Capillary Permeability; Chick Embryo; Chorioallantoic Membrane; Disease Models, Animal; Dose-Response Relationship, Drug; Exudates and Transudates; Inflammation; Male; Mice; Mice, Inbred ICR; Neovascularization, Physiologic; Nitrites; Ubiquinone; Vitamins

Metabolic syndrome (MetS) is a group of cardiovascular risk factors, including visceral obesity, glucose intolerance, hypertension, and dyslipidemia. Increased oxidative and nitrative stress and inflammation and decreased endothelial function occur in an animal model of metabolic syndrome, SHR/NDmcr-cp (SHR/cp) rats. The present study investigated the effects of coenzyme Q10 (CoQ10), one of the important antioxidants, on the abnormal oxidative condition and characteristic components of metabolic syndrome in SHR/cp rats by maintaining them on a diet supplemented with 0.07% - 0.7% CoQ10 for 26 weeks. We determined serum levels of oxidatively modified low-density lipoprotein (Ox-LDL) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) as oxidative stress markers, 3-nitrotyrosine as a nitrative stress marker, 3-chlorotyrosine as a marker of myeloperoxidase (MPO)-catalyzed oxidation and high-sensitivity C-reactive protein (hsCRP) as an inflammatory marker. The administration of CoQ10 significantly attenuated the increase of oxidative and nitrative stress markers and inflammatory markers in a dose-dependent manner. CoQ10 prevented the elevated serum insulin levels, although it did not affect the elevated glucose level and dyslipidemia. CoQ10 also reduced elevated blood pressure, but did not affect body weight gain. In addition, CoQ10 improved endothelial dysfunction in the mesenteric arteries. These findings suggest that the antioxidant properties of CoQ10 can be effective for ameliorating cardiovascular risk in MetS.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Blood Glucose; Body Weight; Deoxyguanosine; Disease Models, Animal; Inflammation; Insulin; Lipids; Lipoproteins, LDL; Metabolic Syndrome; Oxidative Stress; Peroxidase; Rats; Rats, Inbred SHR; Tyrosine; Ubiquinone

Clinical studies demonstrated the efficacy of Coenzyme Q10 (CoQ10) as an adjuvant therapeutic in cardiovascular diseases, mitochondrial myopathies and neurodegenerative diseases. More recently, expression profiling revealed that Coenzyme Q10 (CoQ10) influences the expression of several hundred genes. To unravel the functional connections of these genes, we performed a text mining approach using the Genomatix BiblioSphere. We identified signalling pathways of G-protein coupled receptors, JAK/STAT, and Integrin which contain a number of CoQ10 sensitive genes. Further analysis suggested that IL5, thrombin, vitronectin, vitronectin receptor, and C-reactive protein are regulated by CoQ10 via the transcription factor NFkappaB1. To test this hypothesis, we studied the effect of CoQ10 on the NFkappaB1-dependent pro-inflammatory cytokine TNF-alpha. As a model, we utilized the murine macrophage cell lines RAW264.7 transfected with human apolipoprotein E3 (apoE3, control) or pro-inflammatory apoE4. In the presence of 2.5 microM or 75 microM CoQ10 the LPS-induced TNF-alpha response was significantly reduced to 73.3 +/- 2.8% and 74.7 +/- 8.9% in apoE3 or apoE4 cells, respectively. Therefore, the in silico analysis as well as the cell culture experiments suggested that CoQ10 exerts anti-inflammatory properties via NFkappaB1-dependent gene expression.

Topics: Animals; Cell Line; Computer Simulation; Gene Expression; Inflammation; Lipopolysaccharides; Macrophages; Mice; Models, Biological; Signal Transduction; Tumor Necrosis Factor-alpha; Ubiquinone

Dietary coenzyme Q(10) prolongs life span of rats fed on a PUFAn-6-enriched diet. Our aim was to analyze changes in the levels of plasma proteins of rats fed on a PUFAn-6 plus coenzyme Q(10)-based diet. This approach could give novel insights into the mechanisms of life span extension by dietary coenzyme Q(10) in the rat. Serum albumin, which decreases with aging in the rat, was significantly increased by coenzyme Q(10) supplementation both at 6 and 24 months. After depletion of the most abundant proteins by affinity chromatography, levels of less abundant plasma proteins were also studied by using 2D-electrophoresis and MALDI-TOF mass fingerprinting analysis. Our results have shown that lifelong dietary supplementation with coenzyme Q(10) induced significant decreases of plasma hemopexin, apolipoprotein H and inter-alpha-inhibitor H4P heavy chain (at both 6 and 24 months), preprohaptoglobin, fibrinogen gamma-chain precursor, and fetuin-like protein (at 6 months), and alpha-1-antitrypsin precursor and type II peroxiredoxin (at 24 months). On the other hand, coenzyme Q(10) supplementation resulted in significant increases of serine protease inhibitor 3, vitamin D-binding protein (at 6 months), and Apo A-I (at 24 months). Our results support a beneficial role of dietary coenzyme Q(10) decreasing oxidative stress and cardiovascular risk, and modulating inflammation during aging.

Topics: Animals; Blood Proteins; Cardiovascular Diseases; Coenzymes; Dietary Supplements; Electrophoresis, Gel, Two-Dimensional; Inflammation; Longevity; Male; Oxidative Stress; Proteome; Rats; Rats, Wistar; Ubiquinone

Coenzyme Q10 (CoQ10, ubiquinone) is an essential cofactor in the electron transport chain, serves as a potent antioxidant in mitochondria and lipid membranes, and is often used as a dietary supplement for a number of diseases including cardiovascular diseases. Recently, we obtained evidence that CoQ10 (Kaneka Q10) affects the expression of hundreds of human genes. To decipher the functional and regulatory connections of these genes, a literature search combined with transcription factor binding site analysis was performed using Genomatix BiblioSphere and MatInspector. This in-silico analysis revealed 17 CoQ10-inducible genes which are functionally connected by signalling pathways of G-protein coupled receptors, JAK/STAT, integrin, and beta-arrestin. Promoter analysis of these CoQ10-inducible genes showed one group of NF B-regulated genes, namely IL5, thrombin, vitronectin receptor and C-reactive protein (CRP). Furthermore, a common promoter framework containing binding sites of the transcription factor families EVI1, HOXF, HOXC, and CLOX was identified in the promoters of IL5, CRP, and vitronectin receptor. The identified CoQ10-inducible genes and pathways play an important role in inflammatory response. Since these effects are based on an in-vitro study, the effect of CoQ10 on vascular health in vivo needs to be addressed in further animal and/or human intervention studies.

Topics: Caco-2 Cells; Coenzymes; Computational Biology; Gene Expression Regulation; Humans; Inflammation; Signal Transduction; Software; Ubiquinone

Inflammation and oxidative stress are processes that mark early metabolic abnormalities in vascular diseases.. We explored the effects of a high-fat, high-cholesterol (HFHC) diet on vascular responses in baboons and the potential response-attenuating effects of vitamin E and coenzyme Q(10) (CoQ(10)) supplementation.. We used a longitudinal design by subjecting 21 baboons (Papio hamadryas) to sequential dietary challenges.. After being maintained for 3 mo on a baseline diet (low in fat and cholesterol), 21 baboons were challenged with an HFHC diet for 7 wk. The serum C-reactive protein (CRP) concentrations did not change. Subsequent supplementation of the HFHC diet with the antioxidant vitamin E (250, 500, or 1000 IU/kg diet) for 2 wk reduced serum CRP concentrations from 0.91 +/- 0.02 to 0.43 +/- 0.06 mg/dL. Additional supplementation with CoQ(10) (2 g/kg diet) further reduced serum CRP to approximately 30% of baseline (0.28 +/- 0.03 mg/dL; P = 0.036 compared with the HFHC diet). Introduction of the HFHC diet itself significantly decreased serum P-selectin (from 48.8 +/- 7.2 to 32.9 +/- 3.7 ng/dL, P = 0.02) and von Willebrand factor (from 187.0 +/- 10.1 to 161.9 +/- 9.0%, P = 0.02) concentrations. However, neither vitamin E alone nor vitamin E plus CoQ(10) significantly altered the serum concentrations of P-selectin or von Willebrand factor.. Dietary supplementation with vitamin E alone reduces the baseline inflammatory status that is indicated by the CRP concentration in healthy adult baboons. Cosupplementation with CoQ(10), however, significantly enhances this antiinflammatory effect of vitamin E.

Topics: alpha-Tocopherol; Analysis of Variance; Animals; Antioxidants; Arteriosclerosis; Biomarkers; C-Reactive Protein; Cholesterol, Dietary; Coenzymes; Dietary Fats; Dietary Supplements; Dose-Response Relationship, Drug; Drug Synergism; Female; Inflammation; Longitudinal Studies; Male; Oxidative Stress; P-Selectin; Papio; Random Allocation; Ubiquinone; Vitamin E; von Willebrand Factor

Using a newly developed method by HPLC with ultraviolet detection we measured plasma coenzyme Q10 (CoQ10) level in group of 43 children (19 females and 24 males: ages 1 month-9 years) with an acute inflammatory process. The results for coenzyme Q10 were expressed as molar concentration (mumol/l plasma). Our study confirmed that CoQ10 concentration (median--0.8 mumol/l) was independent of sex, and we established which biochemical parameters influence on ubiquinone levels. The results indicate that CoQ10 concentration is connected with leukocytosis, calcium and magnesium levels. These findings suggested that transferin, amylase and serum glutamic transmainase may also determine the CoQ10 plasma levels.

Topics: Acute Disease; Biomarkers; Blood Chemical Analysis; Child; Child, Preschool; Chromatography, High Pressure Liquid; Coenzymes; Female; Humans; Infant; Inflammation; Male; Oxidation-Reduction; Probability; Prognosis; Sensitivity and Specificity; Severity of Illness Index; Ubiquinone

The levels of Coenzyme Q10 (CoQ10) were determined by HPLC in seminal fluid samples obtained from 77 patients who performed a standard semen analysis for infertility, previous phlogosis or varicocele. CoQ10 was determined in total seminal fluid (n = 60), in seminal plasma (n = 44) and in the cell pellet (n = 37). The molecule, in total fluid, showed a linear correlation with sperm count and motility. In the pellet of spermatozoa, a trend toward an inverse correlation between CoQ10 (expressed as ng/10(6) cells) and semen parameters could be observed. A different pattern was shown in varicocele patients, in whom, in total fluid, the correlation between CoQ10 and sperm count was preserved, but the one between CoQ10 and sperm motility was lacking; moreover, a higher proportion of CoQ10 was present in seminal plasma, and the inverse trend between cellular CoQ10 and sperm count and motility was not observed. These data suggest a pathophysiological role of ubiquinone in human seminal fluid and a molecular defect in the spermatozoa of varicocele patients.

Topics: Adult; Coenzymes; Genital Diseases, Male; Humans; Infertility, Male; Inflammation; Male; Oligospermia; Semen; Sperm Count; Sperm Motility; Ubiquinone; Varicocele