Ginsenoside Rb1 attenuates cardiomyocyte apoptosis induced by myocardial ischemia reperfusion injury through mTOR signal pathway

Biomedicine & Pharmacotherapy

Yu-Wei Pu¹  Yong-Liang Jiang²  Lin Sun²  Li-Qiu Xie²  Zhi Lin²  Di Lu²  Chang-Yan Li³  Ping Yang³ 

[1] Technology Transfer Center, Kunming Medical University, Kunming 650500, China;Department of Cardiology, the Second Affiliated Hospital of Kunming Medical University, Kunming 650101, China;Faculty of Basic Medical Science, Kunming Medical University, Kunming 650500, China;

关键词: Apoptosis;    mTOR;    Myocardial ischemia reperfusion injury;    Ginsenoside Rb1;   

DOI  :  

来源: DOAJ

【 摘 要 】

Objective: Ginsenoside Rb1 (GRb1) is known to play an effective protection on myocardial infarction, yet its therapeutic mechanism on myocardial ischemia/reperfusion (I/R) injury has remained obscure. Here we sought to investigate the protective mechanism of GRb1 preconditioning on myocardial I/R injury in rats. Methods and results: We report here that GRb1 preconditioning could improve myocardial I/R injury induced-cardiac functions including LVDP, -dp/dt min and + dp/dt max; however, the heart rate (HR) was maintained at a level comparable to the I/R group. Additionally, in I/R injury group given GRb1 preconditioning, release of myocardial enzymes (CK-MB and Trop l) and CtsB was decreased. Moreover, GRb1 decreased the expression of apoptotic related proteins e.g. cleaved-caspase 3; however, the ratio of Bcl-2/Bax related to anti-apoptosis was decreased. The study was extended by injecting rapamycin intraperitoneally before GRb1 pretreatment. Thus, mTOR pathway was significantly upregulated after GRb1 pretreatment when compared with I/R. Remarkably, the anti-apoptosis protection of GRb1 pretreatment was attenuated by rapamycin. Furthermore, GRb1 effectively reduced the infarct size thus supporting its role in anti-myocardial I/R injury. Conclusions: It is concluded that GRb1 preconditioning can ameliorate myocardial I/R injury as manifested by the improvement of cardiac function indices; moreover, release of myocardial enzymes, namely, CK-MB, Trop l and CtsB was reduced. More importantly, we have shown that the protective effect of GRb1 against I/R injury induced cardiomyocyte apoptosis is associated with the activation of mTOR signal pathway as evident by the use of rapamycin.

【 授权许可】

Unknown