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Polyphenol (-)-Epigallocatechin Gallate during Ischemia Limits Infarct Size Via Mitochondrial KATP Channel Activation in Isolated Rat Hearts

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Author(s)
Dae-Kyu SongYoungho JangJune Hong KimKook-Jin ChunDeokhee LeeZhelong Xu
Keimyung Author(s)
Song, Dae Kyu
Department
Dept. of Physiology (생리학)
Journal Title
Journal of Korean Medical Science
Issued Date
2010
Volume
25
Issue
3
Keyword
Epigallocatechin GallateKATP ChannelsMyocardial InfarctionMyocardial IschemiaMyocardial Reperfusion Injury
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 (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 mM and 4.0±1.7% in EGCG 10 mM, P<0.001 vs. control 27.2±1.4%). This antiinfarct
effect was totally abrogated by 10 mM GLI (24.6±1.5%, P<0.001 vs. EGCG).
Similarly, 100 mM 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.
Keimyung Author(s)(Kor)
송대규
Publisher
School of Medicine
Citation
Dae-Kyu Song et al. (2010). Polyphenol (-)-Epigallocatechin Gallate during Ischemia Limits Infarct Size Via Mitochondrial KATP Channel Activation in Isolated Rat Hearts. Journal of Korean Medical Science, 25(3), 380–386. doi: 10.3346/jkms.2010.25.3.380
Type
Article
ISSN
1011-8934
DOI
10.3346/jkms.2010.25.3.380
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/34116
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Physiology (생리학)
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