Pachymic acid ameliorates myocardial ischemia and reperfusion injury by attenuating cardiomyocyte apoptosis through the regulation of the mTOR signal pathway

To explore the function and mechanism of Pachymic acid (PA) on myocardial ischemia /reperfusion. TUNEL, flow cytometry, and western blot were performed to detect the apoptosis level in neonatal mice ventricular cells (NMVCs). ATP, ROS, mPTP, JC-1, GSH, GR activity levels were assessed to evaluate the mitochondrial function. Autophagy level was detected by p-mTOR and LC3II fluorescence intensity and autophagy-associated protein level. Cardiac function was determined by Ejection fraction (EF) and shortening fraction (FS). PA inhibited the apoptosis level and recovered the mitochondrial function in NMVCs after hypoxia/reperfusion. Moreover, PA markedly inhibited ischemia-reperfusion (I/R)-induced autophagy by inhibiting the protein and mRNA levels of LC3-II, Beclin1, ATG5, and ATG7 and the number of autophagosomes and by involving the mTOR pathway. An increasing EF and FS indicated the improved cardiac function, and decreasing oxidative stress was found in PA treated group. The results showed that PA blocked excessive autophagy and apoptosis in I/R mice heart or H/R NMVCs, which was mediated by activating the mTOR pathway.