title: Polyphenol (-)-epigallocatechin gallate during ischemia limits infarct size via mitochondrial K(ATP) channel activation in isolated rat hearts.
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.
authors.affiliation: Department of Physiology1, School of Medicine, Keimyung University, Daegu, Korea.
authors.forename: Dae-Kyu
authors.initials: DK
authors.lastname: Song
authors.forename: Youngho
authors.initials: Y
authors.lastname: Jang
authors.forename: June Hong
authors.initials: JH
authors.lastname: Kim
authors.forename: Kook-Jin
authors.initials: KJ
authors.lastname: Chun
authors.forename: Deokhee
authors.initials: D
authors.lastname: Lee
authors.forename: Zhelong
authors.initials: Z
authors.lastname: Xu
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D003652:Decanoic Acids / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D006321:Heart / Q000187:drug effects* / Q000502:physiology / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D006880:Hydroxy Acids / Q000494:pharmacology; D054086:KATP Channels / Q000378:metabolism*; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism; D009203:Myocardial Infarction / Q000473:pathology*; D017202:Myocardial Ischemia / Q000473:pathology*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000889:Anti-Arrhythmia Agents; D000975:Antioxidants; D003652:Decanoic Acids; D006880:Hydroxy Acids; D054086:KATP Channels; D026902:Potassium Channel Blockers; C052853:5-hydroxydecanoic acid; D002392:Catechin; C045651:epigallocatechin gallate; D005905:Glyburide