摘要 : Oxidative stress can play a key role in myocardial necrosis. The present study was designed to investigate the effect of alpha-mangostin (an antioxidant phytonutrient) on mitochondrial dysfunction and endothelial nitric oxide synt... 展开 Oxidative stress can play a key role in myocardial necrosis. The present study was designed to investigate the effect of alpha-mangostin (an antioxidant phytonutrient) on mitochondrial dysfunction and endothelial nitric oxide synthase (eNOS) expression during isoproterenol-induced myocardial necrosis in rats. Induction of rats with isoproterenol (ISO) (150 mg/kg body weight,intraperitoneally) for 2 days resulted in a significant decrease in the activities of respiratory chain enzymes (NADH dehydrogenase and cytochrome c oxidase),tricarboxylic acid cycle enzymes (isocitrate dehydrogenase,succinate dehydrogenase,malate dehydrogenase,and alpha-ketoglutarate dehydrogenase),mitochondrial antioxidants (GPx,GST,SOD,CAT,and GSH),mitochondrial cytochromes (b,c,c1,and aa3),and adenosine triphosphate level. A marked elevation in mitochondrial lipid peroxidation was also observed in ISO-intoxicated rats. Pretreatment with alpha-mangostin (200mg/kg body weight) orally for 8 days significantly attenuated these functional abnormalities and restored normal mitochondrial function,when compared to the ISO-intoxicated group of rats. Cardiac eNOS expression was assessed by Western blot. Cardiac eNOS expression and NO level were significantly suppressed in ISO-intoxicated rats. Pretreatment with alpha-mangostin extenuated ISO-induced diminution of eNOS expression and NO level.Transmission electron microscopic observations also correlated with these biochemical parameters. Hence,these findings conclude the ameliorative potential of alpha-mangostin against ISO-induced biochemical and morphological changes in mitochondria,which might be mediated through the NO pathway and by its ability at quenching free radicals. 收起