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

多酚(-)-表没食子儿茶素没食子酸酯在缺血过程中通过激活大鼠离体心脏的线粒体 K(ATP)通道来限制梗塞面积

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作者:Dae-Kyu Song, Youngho Jang, June Hong Kim, Kook-Jin Chun, Deokhee Lee, Zhelong Xu

Abstract

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 (K(ATP)) 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 K(ATP) channel blocker glibenclamide (GLI) and a selective mitochondrial K(ATP) (mK(ATP)) 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/dt(max), and -dP/dt(min) throughout the experiments among groups. EGCG-treatment significantly reduced myocardial infarction (14.5+/-2.5% in EGCG 1 microM and 4.0+/-1.7% in EGCG 10 microM, P<0.001 vs. control 27.2+/-1.4%). This anti-infarct effect was totally abrogated by 10 microM GLI (24.6+/-1.5%, P<0.001 vs. EGCG). Similarly, 100 microM 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 K(ATP) channels in EGCG-induced cardioprotection. The mK(ATP) channels play a crucial role in the cardioprotection by EGCG.

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