Qiliqiangxin attenuates oxidative stress-induced mitochondrion-dependent apoptosis in cardiomyocytes via PI3K/AKT/GSK3 β signaling pathway.

Qiliqiangxin attenuates oxidative stress-induced mitochondrion-dependent apoptosis in cardiomyocytes via PI3K/AKT/GSK3β signaling pathway. Biol Pharm Bull. 2019 May 28;: Authors: Zhao Q, Li H, Chang L, Wei C, Yin Y, Bei H, Wang Z, Liang J, Wu Y Abstract Qiliqiangxin capsule (QLQX) is a well-known traditional Chinese medicine that exhibits cardioprotective effects in heart failure patients. However, it remains unclear whether and by which mechanism QLQX attenuates oxidative stress-induced mitochondria-dependent myocardial apoptosis. In vivo, SD rats received left anterior descending coronary artery ligation for 4 weeks to establish a model of heart failure after acute myocardial infarction, and then were treated with QLQX for another 4 weeks. We evaluated cardiac function, oxidative stress injury, as well as the expressions of mitochondria-dependent apoptosis and its signaling factors. The results indicated that QLQX protected cardiac function and attenuated oxidative stress-induced myocardial apoptosis. Meanwhile, QLQX elevated the Bcl-2 expression, declined the expressions of Bax, cytochrome c, apoptotic protease activating factor-1 (Apaf-1), cleaved-caspase9 and cleaved-caspase3, and up-regulated the ratios of phospho-AKT/AKT and phospho-GSK3β/GSK3β. In vitro, H9c2 cardiomyocytes were pretreated with QLQX, then exposed to H2O2 for 24 h. QLQX promoted the proliferation of H9c2 cardiomyocytes induced by H2O2 and reversed oxidative...
Source: Biological and Pharmaceutical Bulletin - Category: Drugs & Pharmacology Authors: Tags: Biol Pharm Bull Source Type: research