cyanidin/necrosis

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Cyanidin-3-O-glucoside Induces Apoptosis and Inhibits Migration of Tumor Necrosis Factor-α-Treated Rat Aortic Smooth Muscle Cells.

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Blueberries are rich in anthocyanins (ACNs), which have recently been noted to protect against atherosclerosis development in mice. Cyanidin-3-O-glucoside (C3G), a member of blueberry ACN family, can inhibit the tumor necrosis factor-α (TNF-α)-induced proliferation of vascular smooth muscle cells

Cyanidin 3-O-beta-D-glucoside suppresses nitric oxide production during a zymosan treatment in rats.

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Anthocyanins are used for food color, and they are widely distributed in the human diets, suggesting that we ingest considerable amounts of anthocyanins from plant-based daily diets. We have demonstrated that a typical anthocyanin, cyanidin 3-O-beta-D-glucoside (C3G), suppressed the zymosan-induced

Cyanidin-3-O-glucoside ameliorates diabetic nephropathy through regulation of glutathione pool.

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Diabetic nephropathy (DN) is a common complication of diabetes and the major cause of chronic kidney disease. Cyanidin 3-glucoside (C3G) is the most widespread anthocyanin in nature. In the present study, we aimed to investigate the possible effects of C3G on DN in db/db mice. We found that body

Cyanidin ameliorates endotoxin-induced myocardial toxicity by modulating inflammation and oxidative stress through mitochondria and other factors.

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Cyanidin, an anthocyanin pigment, demonstrates anti-oxidant and anti-inflammatory properties. Here, we examined the mechanistic role of cyanidin in endotoxin induced myocardial injury in inflammation and oxidative stress. In lipopolysaccharide (LPS) induced myocardial injury model, cyanidin

Cyanidin 3-glucoside ameliorates hyperglycemia and insulin sensitivity due to downregulation of retinol binding protein 4 expression in diabetic mice.

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Adipocyte dysfunction is strongly associated with the development of obesity and insulin resistance. It is accepted that the regulation of adipocytokine expression is one of the most important targets for the prevention of obesity and improvement of insulin sensitivity. In this study, we have

Neuroprotective effects of cyanidin 3-O-glucopyranoside on amyloid beta (25-35) oligomer-induced toxicity.

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Recent studies suggest that the oligomers of short amyloid beta (Abeta) peptides such as Abeta(25-35) as well as full-length Abeta peptides (i.e. Abeta(1-40) and Abeta(1-42) peptides) are responsible for synaptic dysfunction and/or neuronal loss in Alzheimer's disease (AD). Among antioxidant

Cyanidin-3-O-β-glucoside combined with its metabolite protocatechuic acid attenuated the activation of mice hepatic stellate cells.

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Previous studies indicated that cyanidin-3-O-β-glucoside (C3G) as a classical anthocyanin exerted an anti-fibrotic effect in the liver, but its bioavailability was quite low. This study was undertaken to explore the restraining effect of C3G and its metabolite protocatechuic acid (PCA) on the

Low Dose of Cyanidin-3-O-Glucoside Alleviated Dextran Sulfate Sodium-Induced Colitis, Mediated by CD169+ Macrophage Pathway.

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Inflammatory bowel disease (IBD) is a chronic disease of the intestinal tract in which excessive activation of inflammatory response is correlated. Cyanidin-3-O-glucoside (C3G) is a powerful anti-inflammatory agent, widely existing in fruits and vegetables. However, the role of C3G has

Cyanidin 3-O-glucoside Chloride Attenuates Streptococcus suis-Induced Inflammation by Inhibiting MAPK and NF-κB Signaling Pathways in Murine Macrophage J774 Cells.

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Streptococcus suis serotype 2 (SS2), considered to be the most frequent and virulent type among identified serotypes, is an important emerging or re-emerging zoonotic pathogen. Inflammation is thought to be a hallmark of SS2 infection, as demonstrated by most clinical symptoms varying from an

Cyanidin 3-O-β-Glucoside Ameliorates Ethanol-Induced Acute Liver Injury by Attenuating Oxidative Stress and Apoptosis: The Role of SIRT1/FOXO1 Signaling.

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The aim of this study was to examine the effects of Cyanidin 3-O-β-glucoside (C3G) on ethanol (EtOH)-induced acute liver injury in mice as well as in cultured hepatic cells exposed to EtOH, with a focus on the involvement of Silent Mating Type Information Regulation 2 Homolog 1 (SIRT1)/Forkhead

Effects of the vegetable polyphenols epigallocatechin-3-gallate, luteolin, apigenin, myricetin, quercetin, and cyanidin in primary cultures of human retinal pigment epithelial cells.

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OBJECTIVE Vegetable polyphenols (bioflavonoids) have been suggested to represent promising drugs for treating cancer and retinal diseases. We compared the effects of various bioflavonoids (epigallocatechin-3-gallate [EGCG], luteolin, apigenin, myricetin, quercetin, and cyanidin) on the physiological

Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity.

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An increased permeability of the intestinal barrier is proposed as a major event in the pathophysiology of conditions characterized by chronic gut inflammation. This study investigated the capacity of pure anthocyanins (AC), and berry and rice extracts containing different types and amounts of AC,

Protective effects of cyanidin-3-O-beta-glucopyranoside against UVA-induced oxidative stress in human keratinocytes.

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Ultraviolet-A (UVA) radiation causes significant oxidative stress because it leads to the generation of reactive oxygen species (ROS), leading to extensive cellular damage and eventual cell death either by apoptosis or necrosis. We evaluated the protective effects of

Potential therapeutic effects of cyanidin-3-O-glucoside on rheumatoid arthritis by relieving inhibition of CD38+ NK cells on Treg cell differentiation.

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CD38+ NK cells are overabundant in rheumatoid arthritis (RA). Cyanidin-3-O-glucoside (C3G) is an inhibitor of CD38. This study investigated the pathogenic role of CD38+ NK cells and the effect of C3G on RA.Rats with bovine type II collagen-induced arthritis

Protecting the heart against ischemia/reperfusion-induced necrosis and apoptosis: the effect of anthocyanins.

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OBJECTIVE It is well known that cardiomyocyte apoptosis contributes to ischemic heart damage. There is also increasing evidence that the polyphenolic compounds of natural origin, such as anthocyanins, may attenuate ischemia/reperfusion injury though the mechanisms of such protection are not clear.

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