curcumin and Vascular-Diseases

Curcumin is the main active constituent of the medicinal plant Curcuma longa L., used traditionally as a medicinal spice in several ancient civilizations. Different preclinical and clinical studies support the anti-inflammatory properties of curcumin in various inflammatory diseases. As inflammation has an essential role in the pathophysiology of many ocular diseases, curcumin has been suggested as a promising therapeutic agent with anti-inflammatory properties. Based on the extent of experimental and clinical evidence, curcumin can exert protective effects against the corneal, uveal, retinal, optic nerve, orbital, and lacrimal gland inflammatory disorders. Herein, the available literature on the beneficial effects of curcumin in inflammatory eye diseases is reviewed. The limitations and future directions of these investigations are also discussed.

Topics: Anti-Inflammatory Agents; Curcumin; Eye Diseases; Inflammation; Plants, Medicinal; Vascular Diseases

The purpose of this review is to provide a concise overview of the polyphenol curcumin for improving arterial health, specifically endothelial function and arterial stiffness, to reduce cardiovascular disease (CVD) risk and to highlight potential mechanisms of action by which curcumin may improve artery function.. The primary findings of this review support the notion for curcumin to improve arterial health both with aging and obesity. There are few clinical trials on curcumin, and those that currently exist are small in scale but provide evidence for curcumin to improve endothelial function in older adults and reduce arterial stiffness in young, obese men. The antioxidant and anti-inflammatory properties of curcumin appear to be important targets of curcumin that are related to improved arterial health. Mechanistic studies have revealed superoxide dismutase, heme oxygenase-1 and nuclear factor erythroid 2-related factor 2 as emerging targets for the beneficial effects of curcumin on the vasculature.. In summary, the efficacy of curcumin for improving arterial function is promising in the limited number of clinical studies performed to date. Still, much investigation is needed to elucidate the effectiveness of curcumin for improving arterial health to lower CVD risk.

Topics: Anti-Inflammatory Agents; Antioxidants; Arteries; Curcumin; Humans; Inflammation; Oxidative Stress; Vascular Diseases; Vascular Stiffness

Clinical manifestations of autosomal dominant polycystic kidney disease (ADPKD), including evidence of vascular dysfunction, can begin in childhood. Curcumin is a polyphenol found in turmeric that reduces vascular dysfunction in rodent models and humans without ADPKD. It also slows kidney cystic progression in a murine model of ADPKD. We hypothesized that oral curcumin therapy would reduce vascular endothelial dysfunction and arterial stiffness in children/young adults with ADPKD.. Enrolled participants were 18±5 (mean ± SD) years, 54% were girls, baseline brachial artery flow-mediated dilation was 9.3±4.1% change, and baseline aortic pulse-wave velocity was 512±94 cm/s. Fifty-seven participants completed the trial. Neither coprimary end point changed with curcumin (estimated change [95% confidence interval] for brachial artery flow-mediated dilation [percentage change]: curcumin: 1.14; 95% confidence interval, -0.84 to 3.13; placebo: 0.33; 95% confidence interval, -1.34 to 2.00; estimated difference for change: 0.81; 95% confidence interval, -1.21 to 2.84;. Curcumin supplementation does not improve vascular function or slow kidney growth in children/young adults with ADPKD.. Curcumin Therapy to Treat Vascular Dysfunction in Children and Young Adults with ADPKD, NCT02494141.. This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2022_02_07_CJN08950621.mp3.

Topics: Adolescent; Child; Curcumin; Double-Blind Method; Endothelium, Vascular; Female; Humans; Male; Polycystic Kidney, Autosomal Dominant; Vascular Diseases; Vascular Stiffness; Young Adult

Vascular endothelial dysfunction is a potential risk factor for cardiovascular disease. This study evaluated the effect of curcumin on factors associated with vascular dysfunction using rats fed a high-sucrose, high-fat (HSF) diet. The experiment included 2 animal feeding phases. In the first feeding phase, male Sprague-Dawley rats were randomly divided into 2 groups: the control group (n = 8) was fed a standard diet (AIN-93G) and the HSF group (n = 24) was fed an HSF diet for 8 weeks to induce obesity. In the second feeding phase, lasting 4 weeks, the HSF group was randomly divided into 3 subgroups: the O group (n = 8) continued feeding on the HSF diet, the OA group (n = 8) had the HSF diet replaced with AIN-93G, and the OC group (n = 8) was fed the HSF diet supplemented with curcumin (300 mg/kg body weight daily). After 8 weeks, the HSF diet significantly elevated levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), insulin, homeostatic model assessment insulin resistance (HOMA-IR), low-density lipoprotein cholesterol (LDL-C), homocysteine (Hcy), C-reactive protein (CRP), vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1) but significantly reduced levels of nitric oxide (NO) and high-density lipoprotein cholesterol (HDL-C). After dietary intervention, the OA and OC groups exhibited significantly lower levels of AST, ALT, HOMA-IR, cholesterol, LDL-C, Hcy, CRP, VCAM-1, and ICAM-1 and higher levels of NO and catalase (CAT) activity compared with the O group. Superoxide dismutase, CAT, and glutathione peroxidase activities were increased in the OA group, while CAT levels were enhanced in the OC group. In conclusion, this study showed that curcumin supplementation and diet modification can inhibit HSF diet-induced vascular dysfunction potentially by enhancing NO production and antioxidant enzyme activities, thereby suppressing inflammation and oxidative damage in the vascular endothelium.

Topics: Alanine Transaminase; Animals; Antioxidants; Aspartate Aminotransferases; Biomarkers; C-Reactive Protein; Cholesterol; Curcumin; Diet, High-Fat; Dietary Sucrose; Endothelium, Vascular; Homocysteine; Inflammation; Insulin; Insulin Resistance; Intercellular Adhesion Molecule-1; Liver; Male; Malondialdehyde; Obesity; Oxidative Stress; Rats; Rats, Sprague-Dawley; Risk Factors; Vascular Cell Adhesion Molecule-1; Vascular Diseases

Mutations in the coding sequence of the X-linked gene MeCP2 (Methyl CpG-binding protein) are present in around 80% of patients with Rett Syndrome, a common cause of intellectual disability in female and to date without any effective pharmacological treatment. A relevant, and so far unexplored feature of RTT patients, is a marked reduction in peripheral circulation. To investigate the relationship between loss of MeCP2 and this clinical aspect, we used the MeCP2 null mouse model B6.129SF1-MeCP2tm1Jae for functional and pharmacological studies. Functional experiments were performed on isolated resistance mesenteric vessels, mounted on a pressurized myograph. Vessels from female MeCP2(+/-) mice show a reduced endothelium-dependent relaxation, due to a reduced Nitric Oxide (NO) availability secondary to an increased Reactive Oxygen Species (ROS) generation. Such functional aspects are associated with an intravascular increase in superoxide anion production, and a decreased vascular eNOS expression. These alterations are reversed by curcumin administration (5% (w/w) dietary curcumin for 21 days), which restores endothelial NO availability, decreases intravascular ROS production and normalizes vascular eNOS gene expression. In conclusion our findings highlight alterations in the vascular/endothelial system in the absence of a correct function of MeCP2, and uncover related cellular/molecular mechanisms that are rescued by an anti-oxidant treatment.

Topics: Animals; Blood Vessels; Curcumin; Disease Models, Animal; Endothelium, Vascular; Female; Gene Expression Regulation, Enzymologic; Immunohistochemistry; Malondialdehyde; Mice; Mice, Inbred C57BL; Mice, Knockout; Nitric Oxide Synthase Type III; Rett Syndrome; RNA, Messenger; Superoxides; Time Factors; Vascular Diseases

Essential oil components from turmeric (Curcuma longa L.) are documented for neuroprotective, anti-cancer, anti-thrombotic and antioxidant effects. The present study aimed to investigate the disease-modifying potential of curcuma oil (C. oil), a lipophilic component from C. longa L., in hyperlipidaemic hamsters. Male golden Syrian hamsters were fed a chow or high-cholesterol (HC) and fat-rich diet with or without C. oil (30, 100 and 300 mg/kg) for 28 d. In HC diet-fed hamsters, C. oil significantly reduced plasma total cholesterol, LDL-cholesterol and TAG, and increased HDL-cholesterol when compared with the HC group. Similar group comparisons showed that C. oil treatment reduced hepatic cholesterol and oxidative stress, and improved liver function. Hyperlipidaemia-induced platelet activation, vascular dysfunction and repressed eNOS mRNA expression were restored by the C. oil treatment. Furthermore, aortic cholesterol accumulation and CD68 expression were also reduced in the C. oil-treated group. The effect of C. oil at 300 mg/kg was comparable with the standard drug ezetimibe. Delving into the probable anti-hyperlipidaemic mechanism at the transcript level, the C. oil-treated groups fed the chow and HC diets were compared with the chow diet-fed group. The C. oil treatment significantly increased the hepatic expression of PPARa, LXRa, CYP7A1, ABCA1, ABCG5, ABCG8 and LPL accompanied by reduced SREBP-2 and HMGCR expression. C. oil also enhanced ABCA1, ABCG5 and ABCG8 expression and suppressed NPC1L1 expression in the jejunum. In the present study, C. oil demonstrated an anti-hyperlipidaemic effect and reduced lipid-induced oxidative stress, platelet activation and vascular dysfunction. The anti-hyperlipidaemic effect exhibited by C. oil seems to be mediated by the modulation of PPARa, LXRa and associated genes involved in lipid metabolism and transport.

Topics: Animals; Anticholesteremic Agents; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Aorta; Cholesterol, Dietary; Cricetinae; Curcuma; Hypercholesterolemia; Jejunum; Liver; Liver X Receptors; Male; Mesocricetus; Nitric Oxide Synthase Type III; Oils, Volatile; Orphan Nuclear Receptors; Oxidative Stress; Phytotherapy; Plant Preparations; Platelet Activation; PPAR alpha; RNA, Messenger; Triglycerides; Vascular Diseases

Neuron loss, glial activation and vascular degeneration are common sequelae of ischemia-reperfusion (I/R) injury in ocular diseases. The present study was conducted to explore the ability of curcumin to inhibit retinal I/R injury, and to investigate underlying mechanisms of the drug effects.. Different dosages of curcumin were administered. I/R injury was induced by elevating the intraocular pressure for 60 min followed by reperfusion. Cell bodies, brn3a stained cells and TUNEL positive apoptotic cells in the ganglion cell layer (GCL) were quantitated, and the number of degenerate capillaries was assessed. The activation of glial cells was measured by the expression level of GFAP. Signaling pathways including IKK-IκBα, JAK-STAT1/3, ERK/MAPK and the expression levels of β-tubulin III and MCP-1 were measured by western blot analysis. Pre-treatment using 0.01%-0.25% curcumin in diets significantly inhibited I/R-induced cell loss in GCL. 0.05% curcumin pre-treatment inhibited I/R-induced degeneration of retinal capillaries, TUNEL-positive apoptotic cell death in the GCL, brn3a stained cell loss, the I/R-induced up-regulation of MCP-1, IKKα, p-IκBα and p-STAT3 (Tyr), and down-regulation of β-tubulin III. This dose showed no effect on injury-induced GFAP overexpression. Moreover, 0.05% curcumin administered 2 days after the injury also showed a vaso-protective effect.. Curcumin protects retinal neurons and microvessels against I/R injury. The beneficial effects of curcumin on neurovascular degeneration may occur through its inhibitory effects on injury-induced activation of NF-κB and STAT3, and on over-expression of MCP-1. Curcumin may therefore serve as a promising candidate for retinal ischemic diseases.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Blotting, Western; Chemokine CCL2; Curcumin; Dose-Response Relationship, Drug; Glial Fibrillary Acidic Protein; Male; Neurons; NF-kappa B; Rats; Rats, Wistar; Reperfusion Injury; Retina; Retinal Ganglion Cells; Retinal Vessels; Signal Transduction; STAT3 Transcription Factor; Time Factors; Tubulin; Vascular Diseases

Curcumin, an Asian spice and food-coloring agent, is known for its anti-oxidant properties. We propose that curcumin can improve diabetes-induced endothelial dysfunction through superoxide reduction.. Diabetes (DM) was induced in rats by streptozotocin (STZ). Daily curcumin oral feeding was started six weeks after the STZ injection. Twelve weeks after STZ injection, mesenteric arteriolar responses were recorded in real time using intravital fluorescence videomicroscopy. Superoxide and vascular protein kinase C (PKC-βII) were examined by hydroethidine and immunofluorescence, respectively.. The dilatory response to acetylcholine (ACh) significantly decreased in DM arterioles as compared to control arterioles. There was no difference among groups when sodium nitroprusside (SNP) was used. ACh responses were significantly improved by both low and high doses (30 and 300 mg/kg, respectively) of curcumin supplementation. An oxygen radical-sensitive fluorescent probe, hydroethidine, was used to detect intracellular superoxide anion (O2●-) production. O2●- production was markedly increased in DM arterioles, but it was significantly reduced by supplementation of either low or high doses of curcumin. In addition, with a high dose of curcumin, diabetes-induced vascular PKC-βII expression was diminished.. Therefore, it is suggested that curcumin supplementation could improve diabetes-induced endothelial dysfunction significantly in relation to its potential to decrease superoxide production and PKC inhibition.

Topics: Acetylcholine; Animals; Antioxidants; Arterioles; Curcuma; Curcumin; Diabetes Mellitus, Experimental; Dietary Supplements; Endothelium, Vascular; Fluorescence; Male; Nitroprusside; Phytotherapy; Plant Extracts; Protein Kinase C; Rats; Rats, Wistar; Reactive Oxygen Species; Superoxides; Vascular Diseases; Vasoconstriction

Curcumin, a yellow polyphenolic compound from the plant Curcuma ionga , is a commonly used spice and coloring agent with beneficial effects of anti-tumor, anti-inflammatory, and antioxidant activities. The objective of this study was to determine the effect of curcumin on homocysteine-induced endothelial dysfunction in a porcine coronary artery model.. Porcine coronary arteries were cut into 5-mm rings, which were incubated for 24 hours either as control rings, with homocysteine (50 micromol/L), curcumin (5 micromol/L), or a combination of curcumin (5 micromol/L) and homocysteine (50 micromol/L). Myograph tension analysis was performed in response to vessel active drugs including thromboxane A2 analog U466419 (contraction), endothelium-dependent vasorelaxation (bradykinin), and endothelium-independent vasorelaxation (sodium nitroprusside). Immunohistochemical staining was performed for endothelial nitric oxide synthase (eNOS). In addition, superoxide anion production was determined by lucigenin-enhanced chemiluminescence.. All groups of porcine coronary artery rings showed no difference in maximal contraction after U46619 challenge. However, endothelium-dependent vasorelaxation in response to 10(-5) mol/L bradykinin was 40% in the homocysteine-treated group, as compared to 73% in the control group (P = .03). Of importance, curcumin could effectively block homocysteine-induced impairment of endothelium-dependent vasorelaxation. All groups showed no difference in endothelium-independent vasorelaxation. In addition, eNOS immunoreactivity was reduced in the homocysteine group, but the combined homocysteine and curcumin group showed eNOS levels comparable to those in the control group. Furthermore, superoxide anion levels of the endothelial layer were significantly increased by 2-fold in homocysteine-treated vessels as compared to control vessels (P = .02), whereas curcumin could block the effect of homocysteine on superoxide anion production.. These data demonstrate that curcumin effectively reverses the endothelial dysfunction induced by homocysteine. In addition, curcumin significantly blocked homocysteine-induced superoxide anion production and eNOS down-regulation. This study suggests a therapeutic role for dietary curcumin in patients with homocysteinemia, thereby reducing cardiovascular morbidity and mortality.. Hyperhomocysteinemia is a significant clinical problem. It is an independent risk factor for cardiovascular diseases. This study provides new information for better understanding the molecular mechanisms of homocysteine-induced vascular injury. More importantly, curcumin, a natural substance, can effectively block the detrimental effect of homocysteine on the vascular system. Thus curcumin could be used in patients with hyperhomocysteinemia, and to prevent cardiovascular diseases.

Topics: Animals; Antioxidants; Arteries; Coronary Vessels; Curcumin; Endothelium, Vascular; Homocysteine; In Vitro Techniques; Models, Animal; Nitric Oxide Synthase; Nitric Oxide Synthase Type III; Superoxides; Swine; Vascular Diseases; Vasodilation