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J Korean Med Sci. 2010 Mar;25(3):380-6. doi: 10.3346/jkms.2010.25.3.380. Epub 2010 Feb 17.

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

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Department of Physiology1, School of Medicine, Keimyung University, Daegu, Korea.


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.


Epigallocatechin Gallate; KATP Channels; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion Injury

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