Publications (2)2.93 Total impact
-
Article: Resveratrol protects adult cardiomyocytes against oxidative stress mediated cell injury.
[show abstract] [hide abstract]
ABSTRACT: Recent studies from our laboratory have showed that resveratrol, a polyphenol found predominantly in grapes rendered strong cardioprotection in animal models of heart disease. The cardioprotection which was observed was primarily associated with the ability of resveratrol to reduce oxidative stress in these models. The aim of the current study was to corroborate the role of resveratrol as an inhibitor of oxidative stress and explore the underlying mechanisms of its action in heart disease. For this purpose, we used a cell model of oxidative stress, the hydrogen peroxide (H(2)O(2)) exposed adult rat cardiomyocytes, which was treated with and without resveratrol (30μM); cardiomyocytes which were not exposed to resveratrol served as controls. Cell injury, cell death and oxidative stress measurements as well as the activities of the major endogenous antioxidants superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were carried out in control and H(2)O(2) exposed cardiomyocytes, treated with and without resveratrol. Pharmacological blockade using specific blockers of the antioxidant enzymes were used to confirm their role in mediating resveratrol action in H(2)O(2) exposed cardiomyocytes. The status of H(2)O(2) and antioxidant enzymes in serum samples from spontaneously hypertensive rats (SHR) treated with and without resveratrol (2.5mg/kg body weight) was also examined. Our results showed significant cell injury and death in H(2)O(2) exposed cardiomyocytes which was prevented upon resveratrol treatment. SOD and CAT activities were decreased in H(2)O(2) exposed adult rat cardiomyocytes; treatment with resveratrol significantly prevented this reduction. However, GPx activity was not altered in the H(2)O(2) exposed cardiomyocytes in comparison to controls. Pharmacological blockade of SOD and/or CAT prevented the beneficial effect of resveratrol. In SHR, H(2)O(2) levels were increased, but CAT activity was decreased, while SOD remained unchanged, when compared to WKY rats; resveratrol treatment significantly prevented the increase in H(2)O(2) levels and the decrease in CAT activities in SHR. Based on our results, we conclude that treatment with resveratrol prevents oxidative stress induced cardiomyocyte injury mainly by preserving the activities of critical antioxidant enzymes. This may be a crucial mechanism by which resveratrol confers cardioprotection.Archives of Biochemistry and Biophysics 05/2012; 527(2):74-80. · 2.93 Impact Factor -
Article: Potential of resveratrol in preventing the development of heart failure
[show abstract] [hide abstract]
ABSTRACT: Heart failure is a leading cause of mortality in North America and most other parts of the world. Its development is secondary to diseases such as hypertension, coronary artery disease, valvular heart disease or cardiomyopathies. Current therapies for preventing heart failure include the use of diuretics, inhibitors of the renin-angiotensin-aldosterone system and β-adrenergic receptor blockers. These treatments have been moderately successful; however, the incidence of heart failure is on the rise. In view of the limited success with existing therapies it has become very important to pursue alternative strategies. One such approach could be the use of food-derived compounds that have medical benefits, and can be administered as dietary supplements. In this context, resveratrol, a polyphenol, found predominantly in grapes and berries, and a major component of red wine, has been recently drawing significant attention for its cardio-protective properties. Current research on resveratrol has focused on examining its potential in preventing or regressing defects in cardiac structure and function in experimental models of heart disease. In this paper, we will discuss the potential of resveratrol as a nutraceutical in preventing the development of heart failure in the future.Current Chemical Biology. 01/2010; Volume 4, Issue 1, 2010, Pages 84-88.
