Cardioprotective effect of polydatin against ischemia/reperfusion injury: Roles of protein kinase C and mito KATP activation

被引：68

作者：

Miao, Qing ^{[1
]}

Wang, Siwang ^{[1
]}

Miao, Shan ^{[1
]}

Wang, Jianbo ^{[1
]}

Xie, Yanhua ^{[1
]}

Yang, Qian ^{[1
]}

机构：

[1] Fourth Mil Med Univ, Sch Pharm, Inst Mat Med, Xian 710032, Shaanxi, Peoples R China

来源：

PHYTOMEDICINE | 2011年 / 19卷 / 01期

关键词：

Polydatin preconditioning; Ischemia/reperfuion; Oxidative injury; PKC; Mito K-ATP; OXIDATIVE STRESS; CHANNELS; MYOCARDIUM; APOPTOSIS;

D O I：

10.1016/j.phymed.2011.06.023

中图分类号：

Q94 [植物学];

学科分类号：

071001 ;

摘要：

Polydatin preconditioning (PPC) has been reported to be protective against brain and intestine ischemia/reperfusion injury (I/R injury), but whether polydatin exerts cardioprotective effect against myocardial ischemia/reperfusion and the underlying mechanisms remain unclear. Previous studies have demonstrated that oxidative stress plays an important role in the process of I/R. Elevation of oxidative agents and decline in anti-oxidant substance would promote I/R. Meanwhile, the activation of PKC signaling seems to mediate the cardioprotective effects of many drugs by alleviating Ca2+ influx. In the present study, we reported for the first time that intravenous administration of polydatin before I/R significantly limited the infarct size, creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) leakage from the damaged myocardium after I/R. The activity of SOD and the content of MDA remarkably changed in the presence of polydatin as well. However, the cardiac function-preserving and myocardial enzymes leakage-limiting effects of polydatin vanished in the presence of PKC inhibitors and mito K-ATP channel blockers. But there was not a significant change in the activity of SOD and MDA content. We therefore conclude that PPC exerts cardioprotective effect by the activation of PKC-K-ATP-dependent signaling and the direct anti-oxidative stress mechanisms. Crown Copyright (C) 2011 Published by Elsevier GmbH. All rights reserved.

引用

页码：8 / 12

页数：5