Vanillic acid prevents altered ion pumps, ions, inhibits Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in myocardial infarcted rats

The present study aims to evaluate the preventive effects of vanillic acid on altered ion pumps, ions and Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in isoproterenol induced myocardial infarcted rats. Male albino Wistar rats were pretreated with vanillic acid (5 mg/kg and 10 mg/kg body weight) daily for 10 days. After the pretreatment, isoproterenol (100 mg/kg body weight) was injected into rats at an interval of 24h for 2 days to induce myocardial infarction. Isoproterenol induced rats significantly increased activities/levels of serum cardiac markers, plasma lipid peroxidation products, serum uric acid and significantly decreased plasma non-enzymatic antioxidants. Furthermore, isoproterenol significantly altered the activities/levels of ion pumps and ions in the heart. The myocardial expressions of apoptotic genes such as Fas-receptor, caspases-8, -9, and -3 were increased in isoproterenol induced rats. There was a significant increase in cardiomyocyte apoptosis observed in isoproterenol induced rats. Pretreatment with vanillic acid (5 mg/kg and 10 mg/kg body weight) to isoproterenol induced rats showed significant effects on all the biochemical and molecular parameters evaluated. Isolated cardiomyocyte viability by trypan blue exclusion staining also correlated with these biochemical findings. Thus, vanillic acid prevented altered ion pumps, ions and inhibited Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in isoproterenol induced myocardial infarcted rats. Our study also revealed that pretreatment with vanillic acid at the dose of 10 mg/kg body weight was more effective than 5 mg/kg body weight. The cardioprotective effects of vanillic acid are associated with its antioxidant mechanisms.