Abstract
Background Cardiomyocyte apoptosis contributes to cardiac complications of alcoholic cardiomyopathy. The aim of this study was to investigate the role of oxidative stress in myocardial cell apoptosis induced by chronic alcohol intake. Methods and results Alcohol induced oxidative stress in the heart as evidenced by a decrease in SOD and GPx activity as well as by an increase in MDA level. Calpain activity was analyzed by Western blotting. Apoptosis and expression of apoptosis regulating proteins Bad, Bcl-x L were analyzed by immunohistochemistry and TUNEL staining. In cultured adult dog ventricular cardiomyocytes, alcohol induced oxidative stress, which induced apoptosis by induction of Ca 2+ dependent calpain activity. These effects of ethanol on cardiomyocytes were abolished by angiotensin II (Ang II) type 1 (AT 1) receptor blockade. In an animal model of alcoholic cardiomyopathy, administration of AT 1 receptor blockade inhibited calpain activation, and decreased apoptosis in the heart. Thus, results suggest the implication of oxidative stress-induced apoptosis in alcoholic cardiomyopathy. Conclusion Alcohol induced apoptosis in alcoholic cardiomyopathy by induction of calpain activity following oxidative stress, which is mediated through the calcium-dependent pathway. Our data suggest that oxidative stress and calpain activation may be important in the development of alcoholic cardiomyopathy and thus may represent a potential therapeutic target for alcoholic cardiomyopathy.
Published Version
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