Ginsenoside Rh2 Exerts a Therapeutic Effect against Myocardial Infarction via Promoting Angiogenesis and Mitochondrial Bioenergetics

, has demonstrated anticancer activity, amelioration of ischemic brain injury, and mitigation of doxorubicin-induced cardiac damage. The cardioprotective effects of Rh2 were evaluated in a mouse model of acute myocardial infarction (AMI). Mice received Rh2 treatment for 14 days postsurgery, and the cardiac function was assessed by echocardiography. Rh2 treatment significantly improved left ventricular function, reduced infarct size, and suppressed cardiac fibrosis in the MI model. Furthermore, it promoted angiogenesis in the border zone, enhanced mitochondrial membrane potential and ATP production, and reduced hypoxia-induced ROS accumulation, excessive mitochondrial fission, and cardiomyocyte apoptosis. In vitro, Rh2 enhanced human umbilical vein endothelial cell (HUVEC) migration in wound-healing assays, an effect associated with an increased level of ERK phosphorylation. These effects were abolished by U0126, an ERK inhibitor. In conclusion, Rh2 protects against MI-induced cardiac injury by improving mitochondrial bioenergetics and activating an ERK-dependent pathway.