Role of Protein Kinase C-ε (PKCε) in Total Salvianolic Acid-induced Cardioprotection

CHEN Wen; GAO Feng-xiang; GUO Li-li; WANG Jie; ZHANG Chen-hao

doi:10.11653/syfj2013120242

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Role of Protein Kinase C-ε (PKCε) in Total Salvianolic Acid-induced Cardioprotection

更新时间：2024-01-04

- Role of Protein Kinase C-ε (PKCε) in Total Salvianolic Acid-induced Cardioprotection
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 19, Issue 12, Pages: 242-245(2013)
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- DOI：10.11653/syfj2013120242
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- Published：2013
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CHEN Wen, GAO Feng-xiang, GUO Li-li, et al. Role of Protein Kinase C-ε (PKCε) in Total Salvianolic Acid-induced Cardioprotection[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(12): 242-245.
DOI：

CHEN Wen, GAO Feng-xiang, GUO Li-li, et al. Role of Protein Kinase C-ε (PKCε) in Total Salvianolic Acid-induced Cardioprotection[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(12): 242-245. DOI： 10.11653/syfj2013120242.

摘要

目的: 研究丹参总酚酸(TSA) 对大鼠心肌缺血再灌注损伤的保护作用

阐明其作用机制。方法: 采用Langendorff离体心脏恒压灌流模型

30只雄性Wistar大鼠随机分为空白对照组、模型组(I/R组)及丹参总酚酸组(TSA组)。空白对照组用Krebs-Henseleit(K-H)液持续灌注100 min;I/R组(K-H液灌流稳定20 min后

停灌40 min

复灌40 min);TSA组(复灌K-H液中含TSA 0.2 g·L-1

其他同I/R组)。动态检测心室内压

测定冠脉流量(CF)及心脏再灌流出液肌酸激酶(CK)活性变化

同时光镜下观察心肌细胞病理组织形态学变化

蛋白免疫印迹法(Western blotting)检测心肌匀浆、细胞胞浆及线粒体蛋白激酶Cε(PKCε)的表达。结果: 与I/R 组相比

TSA能明显改善缺血/再灌后的心功能

增加冠脉流量

减弱冠脉流出液中CK的活性(P<0.05~P<0.01)

可使心肌细胞损伤程度减轻

增加心肌细胞PKCε蛋白表达

并促进PKCε由细胞质向线粒体的转位。结论: TSA对心肌I/R损伤具有明显保护作用

PKCε的激活及转位可能是TSA保护心肌细胞信号传导通路的组成部分。

Abstract

Objective: To investigate the protective mechanism of total salvianolic acid (TSA) against myocardial I/R injury. Method: The models of myocardial ischemia-reperfusion injury in rats were established by Langendorff mathod. 30 male wistar rats were divided into control group

ischemia-reperfusion group and TSA group. The left ventricular pressure(LVP)

coronary flow(CF) were recorded. The creatine kinase (CK) activities in the flow were measured. The morphological changes of cardiocytes in rats were observed by light microscopy. The protein expression of protein kinase C(PKC) ε was analyzed by Western blotting. Result: TSA significantly improved postischemic contractile function

±dp/dtmax

CF and left ventricular end-diastolic pressure(LVEDP) (P<0.05

P<0.01). TSA distinctly reduced the activities of the CK in the flow (P<0.05

P<0.01).TSA could obviously ameliorate cell injury. And TSA could reinforce PKCε translocate from cytosol to mitochondria. Conclusion: TSA protects the heart from I/R injury partially by activating and translocating PKC ε.

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