Cytoprotective Effects Of Resveratrol Research Articles

In VitroEffect of Resveratrol Supplementation on Oxidative Balance and Intercellular Communication of Leydig Cells Subjected to Induced Oxidative Stress

Many studies have revealed that oxidative stress is a primary factor in the pathogenesis of male reproductive system dysfunctions. The strong antioxidant and cytoprotective effects of resveratrol have previously been demonstrated, but its effect in the context of the male reproduction remains unconvincing. To observe the biological activity of resveratrol in protecting the male reproductive function, hydrogen peroxide-induced oxidative stress in Leydig cells was used as a cell model. The aim of the present study was to examine if resveratrol could induce changes in the gap junction intercellular communication (GJIC), nitric oxide production, total oxidant status (TOS) and total antioxidant capacity (TAC) in TM3 Leydig cells subjected to H2O2. The Leydig cells were exposed to a resveratrol treatment (5, 10, 20, 50 and 100 μM) in the presence or absence of H2O2(300/600 μM) during a 24 hin vitroculture. The cell lysates to assess TOS and TAC, NO production were quantified in a culture medium using the Griess method, and the Scrape Loading/Dye Transfer (SL/DT) technique was used for the determination of GJIC in the exposed TM3 Leydig cells. Treatment with higher doses of resveratrol alone led to a significantly increased TOS (p<0.05 with 100 μM) and NO production (p<0.05 with 50 μM and 100 μM), but significantly reduced TAC (p<0.01 with 100 μM) and GJIC (p<0.05 with 100 μM), while the SL/DT evaluation in the cells exposed to resveratrol at concentrations 5 μM (p<0.05) and 10 μM (p<0.01) revealed a significant stimulation of GJIC. The most potent cytoprotective or stimulatory effect of resveratrol in the cells co-exposed to oxidative stress (300 μM H2O2) was observed at a concentration of 10 μM in the case of GJIC, which was manifested by a significant increase in the values (p<0.05) compared to the control group treated with H2O2alone.

Markers of oxidative stress are elevated in exhaled breath condensate of workers in nanocomposites production

We aimed at studying the potential mechanisms in the preventive effect of resveratrol on serum deprivation induced caspase 3 activation on non-transformed cells.Apoptosis was induced by serum deprivation in primary mouse embryonic fibroblasts. Caspase 3 activation, reactive oxygen species production and depolarization of the mitochondrial membrane were measured by fluorescence methods. The involvement of intracellular receptors and autophagy in the effect of resveratrol were analyzed by using specific agonists and antagonists. The role of autophagy was further examined by Western Blot analysis of its protein markers, LC3-II and p62 as well as by acridine orange staining of acidic vacuoles.We found that neither aromatic hydrocarbon receptors nor estrogen receptors play an important role in the cytoprotective effect of resveratrol. Reactive oxygen species production was not significantly altered by either serum deprivation or resveratrol treatment. In the presence of serum deprivation resveratrol however, induced a significant depolarization in mitochondrial membrane potential. The autophagy inhibitor, chloroquine not only eliminated the preventive effect of resveratrol, but also turned it to deleterious suggesting the prominent role of autophagy induction in the cytoprotective effect. Resveratrol did not alter LC3-II expression, but facilitated p62 degradation in serum deprived cells, suggesting its ability to augment the late phase of autophagy and thus promote the autophagic flux.We have demonstrated that resveratrol can protect primary fibroblasts against serum deprivation induced apoptosis by provoking mild mitochondrial stress and consequent up-regulation of autophagic flux.

An Organ System Approach to Explore the Antioxidative, Anti-Inflammatory, and Cytoprotective Actions of Resveratrol.

Resveratrol is a phenolic phytochemical, with a stilbene backbone, derived from edible plants such as grape and peanut. It is a bioactive molecule with physiological effects on multiple organ systems. Its effects range from the neuroprotective to the nephroprotective, including cardiovascular, neuronal, and antineoplastic responses as a part of its broad spectrum of action. In this review, we examine the effects of resveratrol on the following organ systems: the central nervous system, including neurological pathology such as Parkinson's and Alzheimer's disease; the cardiovascular system, including disorders such as atherosclerosis, ischemia-reperfusion injury, and cardiomyocyte hypertrophy; the kidneys, including primary and secondary nephropathies and nephrolithiasis; multiple forms of cancer; and metabolic syndromes including diabetes. We emphasize commonalities in extracellular matrix protein alterations and intracellular signal transduction system induction following resveratrol treatment. We summarize the known anti-inflammatory, antioxidative, and cytoprotective effects of resveratrol across disparate organ systems. Additionally, we analyze the available literature regarding the pharmacokinetics of resveratrol formulations used in these studies. Finally, we critically examine select clinical trials documenting a lack of effect following resveratrol treatment.

Resveratrol Stimulates Mitochondrial Bioenergetics to Protect Retinal Pigment Epithelial Cells From Oxidative Damage

Resveratrol (RSV) alleviates oxidative damage in human adult retinal pigment epithelial (ARPE) cells. Mitochondrial bioenergetics is associated with oxidative stress. The purpose of this study was to examine the role of mitochondrial bioenergetics in the cytoprotective effect of RSV. Its role in protection against the adverse effects of cigarette smoke (CS) in experimental choroidal neovascularization (CNV) was also examined. Cultured ARPE-19 cells were treated with acrolein alone or acrolein with added RSV. Temporal changes in cell viability, expression of the antioxidant protein, and mitochondrial bioenergetics were evaluated. In an animal study, CNV lesions were created in Brown Norway rats by laser-induced photocoagulation. Effects of CS alone or with additional RSV treatment on CNV lesions were quantified by fundus fluorescein angiography. In ARPE-19 cells, RSV rescued acrolein-induced cell death, alongside reversal of acrolein-induced superoxide dismutase expression. Resveratrol increased the mitochondrial bioenergetics, including basal respiratory rate, adenosine triphosphate synthesis via oxidative phosphorylation, and maximal mitochondrial capacity. In animal experiments, CS induced a significant increase in CNV following laser injury, and this increase in CNV was appreciably prevented following peripheral infusion of RSV. Our results indicate that RSV, a major polyphenol found in red wine, exerts protection against acrolein-induced cytotoxicity in human ARPE-19 cells via increases in the mitochondrial bioenergetics. In addition, the antioxidant effect of RSV may contribute to protection against laser-induced CNV in animals exposed to CS. Therefore, RSV might be beneficial for treatment of acrolein-induced or CS-evoked RPE degeneration.

Effects of Resveratrol and trans-3,5,4'-Trimethoxystilbene on Glutamate-Induced Cytotoxicity, Heme Oxygenase-1, and Sirtuin 1 in HT22 Neuronal Cells

Resveratrol (trans-3,5,4’-trihydroxystilbene) has received considerable attention recently for the potential neuroprotective effects in neurodegenerative disorders where heme oxygenase-1 (HO-1) and sirtuin 1 (SIRT1) represent promising therapeutic targets. Resveratrol has been known to increase HO-1 expression and SIRT1 activity. In this study, the effects of resveratrol and trans-3,5,4’-trimethoxystilbene (TMS), a resveratrol derivative, on cytotoxicity caused by glutamate-induced oxidative stress, HO-1 expression, and SIRT1 activation have been investigated by using murine hippocampal HT22 cells, which have been widely used as an in vitro model for investigating glutamate-induced neurotoxicity. Resveratrol protected HT22 neuronal cells from glutamateinduced cytotoxicity and increased HO-1 expression as well as SIRT1 activity in a concentration-dependent manner. Cytoprotec-tion afforded by resveratrol was partially reversed by the specific inhibition of HO-1 expression by HO-1 small interfering RNA and the nonspecific blockage of HO-1 activity by tin protoporphyrin IX, but not by SIRT1 inhibitors. Surprisingly, TMS, a resveratrol derivative with methoxyl groups in lieu of the hydroxyl groups, and trans-stilbene, a non-hydroxylated analog, failed to protect HT22 cells from glutamate-induced cytotoxicity and to increase HO-1 expression and SIRT1 activity. Taken together, our findings suggest that the cytoprotective effect of resveratrol was at least in part associated with HO-1 expression but not with SIRT1 activation and, importantly, that the presence of hydroxyl groups on the benzene rings of resveratrol appears to be necessary for cytoprotection against glutamate-induced oxidative stress, HO-1 expression, and SIRT1 activation in HT22 neuronal cells.

Cytoprotective effects of resveratrol against oxidative stress: [formula omitted] Randi M. Charbonnet, and Mark J.S. Miller. Albany Medical College, Department of Pediatrics, Physiology & Cell Biology, Albany, NY 12208

Cytoprotective effects of resveratrol against oxidative stress: [formula omitted] Randi M. Charbonnet, and Mark J.S. Miller. Albany Medical College, Department of Pediatrics, Physiology & Cell Biology, Albany, NY 12208