Ginsenoside Rg2 attenuates myocardial fibrosis and improves cardiac function after myocardial infarction via AKT signaling pathway.

With the popularization of percutaneous coronary intervention technology in clinical applications, the mortality rate of acute myocardial infarction has been significantly reduced. However, ventricular remodeling following myocardial infarction (MI) has attracted extensive attention for that it can cause malignant arrhythmia, heart failure, and even death. We aimed to investigate the effects of ginsenoside Rg2 on cardiac function and myocardial fibrosis after MI and its potential mechanism. The results demonstrated that ginsenoside Rg2 improved cardiac function and inhibited collagen deposition in mice after MI. In addition, ginsenoside Rg2 reduced the levels of fibrosis-associated genes Collagen I (Col 1), Collagen III (Col 3), and alpha-smooth muscle actin (α-SMA) by activating phosphorylated AKT in angiotensin II-induced cardiac fibroblasts. Taken together, ginsenoside Rg2 improves cardiac function and attenuates cardiac fibrosis via the AKT pathway, suggesting that ginsenoside Rg2 may be a promising drug for the prevention of ventricular remodeling after MI. Abbreviations: MI: myocardial infarction; AMI: acute myocardial infarction; LAD: left anterior descending; ECM: extracellular matrix; Col 1: collagen I; Col 3: collagen III; α-SMA: alpha-smooth muscle actin; ROS: reactive oxygen species; SOD: superoxide dismutase; GSH: glutathione; HO-1: heme oxygenase-1; WST8: water-soluble tetrazolium salt 8.