Picroside?Ⅱ inhibits hypoxia/reoxygenation-induced cardiomyocyte apoptosis by ameliorating mitochondrial function through a mechanism involving a decrease in reactive oxygen species production

摘要

Reactive oxygen species (ROS)?induced mitochondrial dysfunction plays an important role in cardiomyocyte apoptosis during myocardial ischemia/reperfusion (I/R) injury. Picroside?Ⅱ, isolated from Picrorhiza scrophulariiflora Pennell (Scrophulariaceae), has been reported to protect cardiomyocytes from hypoxia/reoxygenation (H/R)?induced apoptosis, but the exact mechanism is not fully clear. The aim of the present study was to explore the protective effects of picroside?Ⅱ on H/R?induced cardiomyocyte apoptosis and the underlying mechanism. In the H9c2 rat cardiomyocyte cell line, picroside?Ⅱ (100?μg/ml) was added for 48?h prior to H/R. The results showed that picroside?Ⅱ markedly inhibited H/R?induced cardiomyocyte apoptosis. In addition, picroside?Ⅱ was also able to decrease the opening degree of mitochondrial permeability transition pore (mPTP), increase the mitochondrial membrane potential, inhibit cytochrome?c release from mitochondria to cytosol and downregulate caspase?3 expression and activity concomitantly with the decreased ROS production. These results suggested that picroside?Ⅱ inhibited H/R?induced cardiomyocyte apoptosis by ameliorating mitochondrial function through a mechanism involving a decrease in ROS production.