QSKL protects against myocardial apoptosis on heart failure via PI3K/Akt-p53 signaling pathway

被引：70

作者：

Chang, Hong ^{[1
,2
]}

Li, Chun ^{[3
]}

Wang, Qiyan ^{[1
]}

Lu, Linghui ^{[1
]}

Zhang, Qian ^{[1
]}

Zhang, Yi ^{[4
]}

Zhang, Na ^{[3
]}

Wang, Yong ^{[1
]}

Wang, Wei ^{[5
]}

机构：

[1] Beijing Univ Chinese Med, Sch Life Sci, Bei San Huan Dong Lu 11, Beijing 100029, Peoples R China

[2] North China Univ Sci & Technol, Tradit Chinese Med Coll, 21 Bohai Rd, Tangshan 063210, Hebei, Peoples R China

[3] Beijing Univ Chinese Med, Modern Res Ctr Tradit Chinese Med, Bei San Huan Dong Lu 11, Beijing 100029, Peoples R China

[4] Beijing Univ Chinese Med, Sch Chinese Mat Med, Bei San Huan Dong Lu 11, Beijing 100029, Peoples R China

[5] Beijing Univ Chinese Med, Bei San Huan Dong Lu 11, Beijing 100029, Peoples R China

来源：

SCIENTIFIC REPORTS | 2017年 / 7卷

基金：

北京市自然科学基金; 中国国家自然科学基金;

关键词：

ATTENUATES CARDIOMYOCYTE APOPTOSIS; ISCHEMIA-REPERFUSION INJURY; INHIBITION; EXPRESSION;

D O I：

10.1038/s41598-017-17163-x

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];

摘要：

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.

引用

页数：13

共 34 条

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