中国体外循环杂志2017，Vol.15Issue(1)：42-46,5.DOI:10.13498/j.cnki.chin.j.ecc.2017.01.11
PKCε信号通路介导甘青铁线莲活性成分APG抗心肌缺血再灌注损伤的机制研究
Compound APG derived from Clematis tangutica ameliorates myocardial ischemia/reperfusion injury via activating PKCε and inhibiting apoptosis
摘要
Abstract
Objective To investigate the protective effects of APG on myocardial ischemia/reperfusion (I/R) injury (IRI) and its possible mechanism.Methods The cultured H9C2 cells were treated with APG for 24 h,and subjected to IRI (I 45 min,R 3 h).After the 3 h reperfusion,cell viability,serum LDH and serum MDA,cell SOD activity,apoptotic index,PKCε expression,Caspase-3 expression,Bax expression and Bcl-2 expression were detected,then the specific inhibitor of PKCε CHE was applied to evaluate the roles of PKCε in this process.Results I/R treatment reduced cell viability significantly,decreased SOD activity and the Bcl-2/Bax ratio,down-regulated PKCε expression,up-regulated LDH levels,MDA levels and Caspase-3 expression (vs the control group,P<0.05).Moreover,APG treatment (both 2 μM/L and 4 μM/L) increased the cell viability,SOD activity and the Bcl-2/Bax ratio,down-regulated LDH levels,MDA levels and Caspase-3 expression,up-regulated PKCε expression in a dose dependent manner (vs the I/R group,P<0.05).In addition,compared with the APG+IR group,CHE treatment reduced the cell viability,up-regulated Caspase-3 expression,decreased the Bcl-2/Bax ratio (vs the APG+I/R group,P<0.05).Conclusion APG treatment ameliorates I/R injury via activating PKCε pathway and inhibiting apoptosis.关键词
甘青铁线莲/心肌缺血再灌注损伤/蛋白激酶Cε/细胞凋亡Key words
Clematis tangutica/Myocardial ischemia/reperfusion injury/PKCε/Apoptosis引用本文复制引用
冯颖达,冯建宇,杨阳,狄守印,张伟,陆云阳,汤海峰,朱艳荣..PKCε信号通路介导甘青铁线莲活性成分APG抗心肌缺血再灌注损伤的机制研究[J].中国体外循环杂志,2017,15(1):42-46,5.基金项目
国家自然科学基金(81403182,81503285,81570231) （81403182,81503285,81570231）
