Taohong siwu decoction suppresses oxidative stress-induced myocardial apoptosis post-myocardial infarction by inhibiting PTEN pathway

Myocardial infarction (MI) is an important factor inducing mortality globally. Apoptosis and oxidative stress have been identified as major drivers for MI development. Anti-apoptosis therapies exhibit promising effects in protecting against MI. Typically, Taohong Siwu Decoction (THSWD) exerts cardioprotective properties. However, whether THSWD suppresses oxidative stress-induced myocardial apoptosis after MI and the associated mechanisms remain unclear. The present work focused on examining the protective effects of THSWD on oxidative stress-induced myocardial apoptosis after MI and its possible mechanisms. The MI mouse model was established via left anterior descending coronary artery (LAD) ligation. Thereafter, echocardiography and histopathology were performed to examine the cardioprotective effects of THSWD. Meanwhile, the protective potential of THSWD against myocardial apoptosis and oxidative stress, as well as modulation of phosphatase and tensin homolog (PTEN) pathway in MI were investigated through TUNEL staining, ROS analysis, immunohistochemistry (IHC), Western blot (WB) and oxidative stress-related biochemical enzyme assay, respectively. Further, the apoptosis of neonatal cardiomyocytes (NCMs) and H9C2 cells was induced by TBHP in vitro. Thereafter, the impacts of THSWD on the TBHP-induced H9C2 and NCMs were detected by Hoechst33342/PI fluorescent staining, WB, ROS analysis, and oxidative stress-related biochemical enzyme assay. In addition, PTEN was overexpressed using transfection viruses in vivo and in vitro for further investigation. THSWD might inhibit PTEN and promote the PI3K/AKT pathway in MI mice to prevent myocardial apoptosis. In vitro, THSWD prevented the TBHP-induced apoptosis of NCMs and H9C2 cells. This was achieved by blocking PTEN activity and regulating PI3K/AKT pathway. Moreover, PTEN overexpression significantly enhanced the TBHP-induced H9C2 apoptosis and oxidative stress-induced myocardial apoptosis after MI, and partially blocked the protection of THSWD against myocardial apoptosis and modulating PI3K/AKT pathway in vitro and in vivo. THSWD suppressed oxidative stress-induced myocardial apoptosis in vitro and in vivo by inhibiting PTEN pathway.