Protective Effects of Lophanic Acid from Rabdosia lophanthoides on H9c2 Cardiomyocytes Against Hypoxia/Reoxygenation-Induced Apoptosis

Myocardial infarct is a severe cause of death worldwide, which results from the myocardial ischemia and reperfusion injury. Oxidative stress has been triggered in timely reperfusion due to overproduction of reactive oxygen species (ROS) and results in the apoptosis of cardiomyocytes. To discover novel drugs targeting myocardial infarct, we have evaluated the protective effects of lophanic acid (LA) using H9c2 cardiomyocytes injured by hypoxia/restoration (H/R) and explored the possible mechanisms. As a result, LA can protect H9c2 cardiomyocytes against apoptosis induced by H/R. The protection is associated with the inhibition of oxidative stress via reducing ROS generation and MDA content as well as elevating SOD activity. Meanwhile, the improvement of mitochondrial dysfunction through suppressing intracellular calcium overload, attenuating collapse of mitochondrial membrane potential and blocking mitochondrial permeability transition pore opening was observed. These results can give evidences for further investigation on LA in vivo and potential application in practice.