Polyphenol (-)-epigallocatechin gallate during ischemia limits infarct size via mitochondrial K(ATP) channel activation in isolated rat hearts.

Polyphenol (-)-epigallocatechin gallate during ischemia limits infarct size via mitochondrial K(ATP) channel activation in isolated rat hearts.
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DOI:
10.3346/jkms.2010.25.3.380
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发表时间:
2010-03
影响因子:
4.5
通讯作者:
Xu Z
Xu Z
中科院分区:
医学4区
文献类型:
--
作者:
Song DK;Jang Y;Kim JH;Chun KJ;Lee D;Xu Z

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茶多酚(-)-表没食子儿茶素没食子酸酯(EGCG),最丰富的儿茶素的绿色茶,似乎减轻心肌缺血/再灌注损伤。我们研究了ATP敏感性钾(KATP)通道参与EGCG诱导的心脏保护作用。离体大鼠心脏进行30分钟的区域缺血和2小时的再灌注。从缺血前10 min开始至缺血结束,再灌注40 min。非选择性KATP通道阻断剂格列本脲(GLI)和选择性线粒体KATP(mKATP)通道阻断剂5-羟基癸酸(HD)灌注在EGCG处理的心脏。在整个实验过程中,各组之间的冠状动脉流量和心脏动力学(包括心率、左室发展压、心率-血压乘积、+dP/dtmax和-dP/dtmin)无差异。EGCG治疗显著减少心肌梗死(14.5±2.5%,1 µM和4.0±1.7%,10 µM,P<0.001,对照组27.2±1.4%)。这种抗梗死作用被10 µM GLI完全消除(24.6± 1.5%,P<0.001 vs. EGCG)。类似地,100 µM HD也中止了EGCG的抗梗死作用(24.1± 1.2%,P<0.001 vs. EGCG)。这些数据支持KATP通道在EGCG诱导的心脏保护中的作用。mKATP通道在EGCG的心肌保护作用中起着重要作用。
Polyphenol (-)-epigallocatechin gallate (EGCG), the most abundant catechin of green tea, appears to attenuate myocardial ischemia/reperfusion injury. We investigated the involvement of ATP-sensitive potassium (KATP) channels in EGCG-induced cardioprotection. Isolated rat hearts were subjected to 30 min of regional ischemia and 2 hr of reperfusion. EGCG was perfused for 40 min, from 10 min before to the end of index ischemia. A nonselective KATP channel blocker glibenclamide (GLI) and a selective mitochondrial KATP (mKATP) channel blocker 5-hydroxydecanoate (HD) were perfused in EGCG-treated hearts. There were no differences in coronary flow and cardiodynamics including heart rate, left ventricular developed pressure, rate-pressure product, +dP/dtmax, and -dP/dtmin throughout the experiments among groups. EGCG-treatment significantly reduced myocardial infarction (14.5±2.5% in EGCG 1 µM and 4.0±1.7% in EGCG 10 µM, P<0.001 vs. control 27.2±1.4%). This anti-infarct effect was totally abrogated by 10 µM GLI (24.6±1.5%, P<0.001 vs. EGCG). Similarly, 100 µM HD also aborted the anti-infarct effect of EGCG (24.1±1.2%, P<0.001 vs. EGCG ). These data support a role for the KATP channels in EGCG-induced cardioprotection. The mKATP channels play a crucial role in the cardioprotection by EGCG.
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