myricitrin and Inflammation

In humans, oxidative stress is thought to be involved in the development of Parkinson's disease, Alzheimer's disease, atherosclerosis, heart failure, myocardial infarction and depression. Myricitrin, a botanical flavone, is abundantly distributed in the root bark of Myrica cerifera, Myrica esculenta, Ampelopsis grossedentata, Nymphaea lotus, Chrysobalanus icaco, and other plants. Considering the abundance of its natural sources, myricitrin is relatively easy to extract and purify. Myricitrin reportedly possesses effective anti-oxidative, anti-inflammatory, and anti-nociceptive activities, and can protect a variety of cells from in vitro and in vivo injuries. Therefore, our current review summarizes the research progress of myricitrin in cardiovascular diseases, nerve injury and anti-inflammatory, and provides new ideas for the development of myricitrin.

Topics: Alzheimer Disease; Animals; Anti-Inflammatory Agents; Cardiovascular Diseases; Flavonoids; Humans; Inflammation; Myrica; Osteoporosis; Oxidative Stress; Parkinson Disease; Phytotherapy

Inflammation is a biological function which triggered after the mechanical tissue disruption or from the responses by the incidence of physical, chemical or biological negotiator in body. These responses are essential act provided by the immune system during infection and tissue injury to maintain normal tissue homeostasis. Inflammation is a quite complicated process at molecular level with the involvement of several proinflammatory expressions. Several health problems are associated with prolonged inflammation, which effects nearly all major to minor diseases. The molecular and epidemiological studies jagged that the inflammation is closely associated with several disorders with their specific targets. It would be great achievement for human health around the world to overcome on inflammation. Mostly used anti-inflammatory drugs are at high risk of side effects and also expensive. Hence, the plant-based formulations gained a wide acceptance by the public and medical experts to treat it. Due to extensive dispersal, chemical diversity and systematically established biological potentials of natural products have induced renewed awareness as a gifted source for medications. However, today's urgent need to search for cheaper, more potent and safe anti-inflammatory medications to overcome on current situation. The goal of this review to compile an update on inflammation, associated diseases, molecular targets, inflammatory mediators and role of natural products. The entire text concise the involvement of various cytokines in pathogenesis of various human disorders. This assignment discussed about 321 natural products with their promising anti-inflammatory potential discovered during January 2009 to December 2018 with 262 citations.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Biological Products; Cardiovascular Diseases; Humans; Inflammation; Neoplasms; Skin Diseases

Topics: Animals; Cell Line; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Flavonoids; Hypoglycemic Agents; Inflammation; Male; Myrica; Oxidative Stress; Plant Bark; Rats; Rats, Wistar

Osteoarthritis (OA) is a clinical disease which seriously affects the quality of life of sufferers. Although the pathogenesis of OA has not been fully unraveled, it is may be due to increased levels of pro-inflammatory cytokines, activation of inflammation-related signaling pathways, and degradation of extracellular matrix. Osteoarthritis is characterized by chronic joint pain, swelling, stiffness, limited movement or joint deformity, all of which seriously affect the quality of life and health of the affected individuals. Myroside (Myr) is a polyphenolic hydroxyflavone glycoside extracted from the fruits, bark and leaves of myroside and other natural plants. It has many pharmacological properties, especially anti-inflammatory effects. In the present study, primary chondrocytes of IL-1β rats were used to simulate pathological environment of chondrocytes in OA, and to explore the effect of Myr on chondrocytes. It was found that Myr improved the viability and proliferation of chondrocytes, and also inhibited apoptosis in these cells. Moreover, Myr reduced the expressions of inflammatory factors, and inhibited inflammatory reactions in chondrocytes. These findings provide good experimental basis for the clinical application of Myr in the prevention and treatment of progressive degeneration of cartilage in OA.

Topics: Animals; Apoptosis; bcl-2-Associated X Protein; Caspase 3; Caspase 9; Cell Proliferation; Cell Survival; Chondrocytes; Flavonoids; Inflammation; Inflammation Mediators; Interleukin-1beta; Osteoarthritis; Rats; Tumor Necrosis Factor-alpha

The flavonoid myricitrin exhibits various pharmacological and physiological effects. However, studies on the effects of myricitrin on obesity are limited. We hypothesized that dietary myricitrin would attenuate the adiposity and metabolic dysfunction that occur in obesity. To test this hypothesis, mice were randomly fed a high-fat diet (HFD) or HFD supplemented with myricitrin for 16 weeks. Myricitrin significantly reduced white adipose tissue (WAT) mass, adipocyte size, and plasma leptin levels, and also attenuated dyslipidemia. These changes appeared to result from increased energy expenditure and activation of the carnitine acyltransferase (CPT) and

Topics: Adipose Tissue, White; Adiposity; Animals; Diet, High-Fat; Dietary Supplements; Dyslipidemias; Fatty Liver; Flavonoids; Inflammation; Insulin Resistance; Leptin; Liver; Male; Mice; Mice, Inbred C57BL; Obesity

The present investigation determined the protective effect of myricitrin against sepsis-associated encephalopathy in rats.. Sepsis was induced by cecal ligation and puncture (CLP); rats were treated with 30 or 100 mg/kg of myricitrin for 5 days prior to the induction of CLP. The effect of myricitrin was observed by determining the neurological function using the open field test and step-down inhibitory avoidance test. Cerebral oedema and the levels of inflammatory and oxidative stress mediators were determined in brain tissues. Moreover, the expression levels of Bcl-2, Bax, IκB-α, nuclear factor κB (NF-κB), caspase-3 and NLRP3 were estimated in brain tissues by Western blotting and the mRNA expression of NF-κB, caspase-3 and NLRP3 in brain tissues was estimated by real-time polymerase chain reaction. An immunofluorescence assay was performed to estimate inflammasome activity.. The results suggest that treatment with myricitrin protects neuronal function in rats with CLP-induced sepsis. Decreases in inflammation and oxidative stress mediators were observed in the brain tissues of the myricitrin-treated group compared to the CLP group. Moreover, treatment with myricitrin ameliorated the altered Bcl-2, Bax, IκB-α, NF-κB, caspase-3 and NLRP3 protein and mRNA expression levels in the brain tissues of septic rats.. The data reveal that myricitrin ameliorated neuroinflammation and improved memory in rats with CLP-induced sepsis by regulating the NLRP3/Bax/Bcl signalling pathway.

Topics: Animals; Flavonoids; Inflammation; Male; Memory; NF-kappa B; NLR Family, Pyrin Domain-Containing 3 Protein; Oxidative Stress; Rats, Wistar; Sepsis; Sepsis-Associated Encephalopathy

Chronic fatigue patients experience various neuropsychological symptoms, including fatigue behaviors, chronic pain, and depression. They also display immune system dysregulation. Polygonum aviculare L. extract (PAE) is a traditional herbal medicine used to treat inflammatory diseases by reportedly decreasing pro-inflammatory cytokine production.. We hypothesized that the anti-inflammatory properties of PAE would attenuate fatigue symptoms in a mouse model of restraint stress.. We evaluated the effects of PAE on fatigue using three experimental groups: unstressed, vehicle-treated stressed, and PAE-treated stressed mice. This restraint stress paradigm, comprised of restraint for 3 h daily for 15 days, was used to model chronic fatigue.. We compared lethargy-like behavior between our experimental groups using forced-swim, sucrose preference, and open-field tests once per week on days 7 and 14 of restraint stress. We also used histology and western blotting to evaluate pro-inflammatory cytokine expression in the brain and serum, and microglial activation in the brain. Finally, we used liquid chromatography/mass spectroscopy (LC/MS) to identify individual components of PAE, and applied cell culture techniques to test the effects of these components on neuronal cells in vitro.. In restraint-stressed mice, PAE treatment decreased lethargy-like behavior relative to vehicle-treated animals. PAE treatment also reduced expression of fatigue-related factors such as corticosterone, serotonin, and catecholamines (adrenaline and noradrenaline) in the brain and serum, and decreased expression of CD68, Ibal-1, and the inflammatory cytokines TNF-α, IL-6, and IL-1β in the brain. Together, these data indicate that PAE reduced fatigue and is anti-inflammatory. Furthermore, histopathological analyses indicated that PAE treatment recovered atrophic volumes and hepatic injuries. Finally, LC/MS analysis of PAE identified four individual chemicals: myricitrin, isoquercitrin, avicularin, and quercitrin. In neuronal cell cultures, treatment with these PAE components inhibited TNF-α production, confirming that PAE treatment reduces neuroinflammation.. PAE treatment may reduce fatigue by suppressing neuroinflammation and the expression of fatigue-related hormones.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Brain; Corticosterone; Cytokines; Disease Models, Animal; Drugs, Chinese Herbal; Fatigue; Flavonoids; Inflammation; Male; Mice, Inbred C57BL; Plant Extracts; Polygonum; Serotonin; Stress, Physiological

Diabetic cardiomyopathy (DCM) has been increasingly considered as a main cause of heart failure and death in diabetic patients. At present, no effective treatment exists to prevent its development. In the present study, we describe the potential protective effects and mechanisms of myricitrin (Myr) on the cardiac function of streptozotosin-induced diabetic mice and on advanced glycation end products (AGEs)-induced H9c2 cardiomyocytes. In vitro experiments revealed that pretreatment with Myr significantly decreased AGEs-induced inflammatory cytokine expression, limited an increase in ROS levels, and reduced cell apoptosis, fibrosis, and hypertrophy in H9c2 cells. These effects are correlated with Nrf2 activation and NF-κB inhibition. In vivo investigation demonstrated that oral administration of Myr at 300 mg/kg/day for 8 weeks remarkably decreased the expression of enzymes associated with cardiomyopathy, as well as the expression of inflammatory cytokines and apoptotic proteins. Finally, Myr improved diastolic dysfunction and attenuated histological abnormalities. Mechanistically, Myr attenuated diabetes-induced Nrf2 inhibition via the regulation of Akt and ERK phosphorylation in the diabetic heart. Collectively, these results strongly indicate that Myr exerts cardioprotective effects against DCM through the blockage of inflammation, oxidative stress, and apoptosis. This suggests that Myr might be a potential therapeutic agent for the treatment of DCM.

Topics: Animals; Apoptosis; Cell Line; Diabetic Cardiomyopathies; Flavonoids; Inflammation; Mice; Mice, Inbred BALB C; Myocytes, Cardiac; Oxidative Stress

This protocol describes microsphere-based protease assays for use in flow cytometry and high-throughput screening. This platform measures a loss of fluorescence from the surface of a microsphere due to the cleavage of an attached fluorescent protease substrate by a suitable protease enzyme. The assay format can be adapted to any site or protein-specific protease of interest and results can be measured in both real time and as endpoint fluorescence assays on a flow cytometer. Endpoint assays are easily adapted to microplate format for flow cytometry high-throughput analysis and inhibitor screening.

Topics: Animals; Biotinylation; Flow Cytometry; Fluorescence Resonance Energy Transfer; Green Fluorescent Proteins; High-Throughput Screening Assays; Humans; Inflammation; Kinetics; Microspheres; Peptide Hydrolases; Peptides; Reproducibility of Results; Temperature

Flavonoids are increasingly being ingested by the general population as chemotherapeutic and anti-inflammatory agents. They are potentially toxic because of their conversion to free radicals and reactive quinones by peroxidases. Little detailed information is available on how flavonoids interact with myeloperoxidase, which is the predominant peroxidase present at sites of inflammation. This enzyme uses hydrogen peroxide to oxidize chloride to hypochlorous acid, as well as to produce an array of reactive free radicals from organic substrates. We investigated how the flavonoid myricitrin is oxidized by myeloperoxidase and how it affects the activities of this enzyme. Myricitrin was readily oxidized by myeloperoxidase in the presence of hydrogen peroxide. Its main oxidation product was a dimer that underwent further oxidation. In the presence of glutathione, myricitrin was oxidized to a hydroquinone that was conjugated to glutathione. When myeloperoxidase oxidized myricitrin and related flavonoids it became irreversibly inactivated. The number of hydroxyl groups in the B ring of the flavonoids and the presence of a free hydroxyl m-phenol group in the A ring were important for the inhibitory effects. Less enzyme inactivation occurred in the presence of chloride. Neutrophils also oxidized myricitrin to dimers in a reaction that was partially dependent on myeloperoxidase. Myricitrin did not affect the production of hypochlorous acid by neutrophils. We conclude that myricitrin will be oxidized by neutrophils at sites of inflammation to produce reactive free radicals and quinones. It is unlikely to affect hypochlorous acid production by neutrophils.

Topics: Apoptosis; Chromatography, High Pressure Liquid; Enzyme Activation; Flavonoids; Free Radicals; Glutathione; Humans; Hypochlorous Acid; In Vitro Techniques; Inflammation; Neutrophils; Oxidation-Reduction; Peroxidase; Structure-Activity Relationship; Substrate Specificity

The aim of the present study was to investigate the effects of myricitrin, a flavonoid with anti-inflammatory and antinociceptive action, upon persistent neuropathic and inflammatory pain. The neuropathic pain was caused by a partial ligation (2/3) of the sciatic nerve and the inflammatory pain was induced by an intraplantar (i.pl.) injection of 20 microL of complete Freund's adjuvant (CFA) in adult Swiss mice (25-35 g). Seven days after sciatic nerve constriction and 24 h after CFA i.pl. injection, mouse pain threshold was evaluated through tactile allodynia, using Von Frey Hair (VFH) filaments. Further analyses performed in CFA-injected mice were paw edema measurement, leukocytes infiltration, morphological changes and myeloperoxidase (MPO) enzyme activity. The intraperitoneal (i.p.) treatment with myricitrin (30 mg/kg) significantly decreased the paw withdrawal response in persistent neuropathic and inflammatory pain and decreased mouse paw edema. CFA injection increased 4-fold MPO activity and 27-fold the number of neutrophils in the mouse paw after 24 h. Myricitrin strongly reduced MPO activity, returning to basal levels; however, it did not reduce neutrophils migration. In addition, myricitrin treatment decreased morphological alterations to the epidermis and dermis papilar of mouse paw. Together these results indicate that myricitrin produces pronounced anti-allodynic and anti-edematogenic effects in two models of chronic pain in mice. Considering that few drugs are currently available for the treatment of chronic pain, the present results indicate that myricitrin might be potentially interesting in the development of new clinically relevant drugs for the management of this disorder.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Disease Models, Animal; Edema; Female; Flavonoids; Freund's Adjuvant; Inflammation; Mice; Neutrophil Infiltration; Pain; Pain Threshold; Sciatic Neuropathy; Subcutaneous Tissue