Abstract
The ancient traditional Chinese medicine Qishenkeli (QSKL) is widely used in the treatment of heart failure (HF) in China. Previous studies have shown that QSKL has definite effects on HF. The purpose of this study is to identify the regulation of QSKL on apoptosis and clarify the underlying mechanism. An apoptosis model of H9C2 cells was induced by oxygen-glucose deprivation/recovery (OGD/R). An animal model of HF was induced by ligation of left anterior descending (LAD) coronary artery in rat. We found that QSKL reduced intracellular ROS generation, increased mitochondrial membrane potential and protected H9C2 cells against OGD/R-induced apoptosis. In vivo results showed that QSKL administration could improve cardiac functions, decrease fibrotic area, infarct size and apoptotic rate in HF model. QSKL regulated the expressions of key apoptotic molecules, including increasing Bcl-2/Bax ratio, reducing the expressions of P53, Bax and Cleaved-caspase-3. Interestingly, QSKL also regulated the phosphorylated expressions of PI3K and Akt without significantly affecting PTEN. Taken together, the protective and anti-apoptotic effects of QSKL could be mediated partly through modulating the PI3K/Akt-P53 apoptotic pathway.
Highlights
Heart failure (HF), a terminal stage of most cardiovascular diseases, has been recognized as a refractory condition worldwide
Apoptosis has been shown to play an important role in the progression of heart failure
We demonstrated that QSKL could exert cardio-protective effect by attenuating cardiac apoptosis
Summary
Heart failure (HF), a terminal stage of most cardiovascular diseases, has been recognized as a refractory condition worldwide. Cardiomyocytes apoptosis occurs in the development of various cardiovascular diseases, such as myocardial infarction and ischemia/reperfusion[2,3]. P53 could up-regulate Bax expression, and inhibit the anti-apoptotic effect of Bcl-2 by directly combining with it[7]. Studies have found that dysregulation of P53 is related to the progression of various cardiovascular diseases, such as ischemia/reperfusion, heart failure, atherosclerosis, etc[9,10,11]. Previous studies showed that the mechanisms of QSKL in preventing HF may be mediated through attenuating oxidative stress, inhibiting inflammation and regulating renin-angiotensin-aldosterone system (RAAS)[12,13,14]. A heart failure (HF) rat model and an apoptotic H9C2 cell model were induced to investigate the underlying mechanisms of QSKL on inhibiting myocardial apoptosis
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