Coptisine alleviates ischemia/reperfusion-induced myocardial damage by regulating apoptosis-related proteins

Coptisine is an alkaloid with many biological functions, but studies on its mechanism in myocardial ischemia-reperfusion (I/R) injury are less reported. Hypoxia-reoxygenation (H/R) -treated cardiomyocytes injury and I/R-induced myocardial tissues damage were created in rat models with or without the pre-treatment of coptisine. The proliferation and apoptosis of cardiomyocytes and changes of myocardial tissues were observed after the pre-treatment of coptisine. The pre-treatment of coptisine promoted cell proliferation and inhibited apoptosis of H/R-injured cardiomyocytes, and alleviated the myocardial tissue injury caused by I/R in rats. Moreover, coptisine promoted the expressions of anti-apoptotic proteins and inhibited the expressions of pro-apoptotic proteins in vivo and in vitro. The current study found that coptisine had protective effects on I/R-induced myocardial damage, which may provide a new insight into the treatment of I/R.