Polyphenol (-)-Epigallocatechin Gallate during Ischemia Limits Infarct Size Via Mitochondrial K(ATP) Channel Activation in Isolated Rat Hearts.
10.3346/jkms.2010.25.3.380
- Author:
Dae Kyu SONG
1
;
Youngho JANG
;
June Hong KIM
;
Kook Jin CHUN
;
Deokhee LEE
;
Zhelong XU
Author Information
1. Department of Physiology1, School of Medicine, Keimyung University, Daegu, Korea.
- Publication Type:Original Article
- Keywords:
Epigallocatechin Gallate;
KATP Channels;
Myocardial Infarction;
Myocardial Ischemia;
Myocardial Reperfusion Injury
- MeSH:
Animals;
Anti-Arrhythmia Agents/pharmacology;
Antioxidants/*pharmacology;
Catechin/*analogs & derivatives/pharmacology;
Decanoic Acids/pharmacology;
Glyburide/pharmacology;
Heart/*drug effects/physiology/physiopathology;
Hemodynamics;
Humans;
Hydroxy Acids/pharmacology;
KATP Channels/*metabolism;
Male;
Mitochondria, Heart/*drug effects/metabolism;
Myocardial Infarction/*pathology;
Myocardial Ischemia/*pathology;
Potassium Channel Blockers/pharmacology;
Rats;
Rats, Wistar
- From:Journal of Korean Medical Science
2010;25(3):380-386
- CountryRepublic of Korea
- Language:English
-
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 micrometer and 4.0+/-1.7% in EGCG 10 micrometer, P<0.001 vs. control 27.2+/-1.4%). This anti-infarct effect was totally abrogated by 10 micrometer GLI (24.6+/-1.5%, P<0.001 vs. EGCG). Similarly, 100 micrometer 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.
