Polyphenol (-)-epigallocatechin gallate-induced cardioprotection may attenuate ischemia-reperfusion injury through adenosine receptor activation: a preliminary study.
10.4097/kjae.2012.63.4.340
- Author:
Sang Kwon LEE
1
;
June Hong KIM
;
Jeong Su KIM
;
Youngho JANG
;
Jun KIM
;
Yong Hyun PARK
;
Kook Jin CHUN
;
Mi Young LEE
Author Information
1. Department of Thoracic and Cardiovascular Surgery, Pusan National University Yangsan Hospital, Yangsan, Korea.
- Publication Type:Original Article
- Keywords:
Adenosine;
Epigallocatechin gallate;
Myocardial infarction;
Reperfusion injury
- MeSH:
Adenosine;
Animals;
Catechin;
Guanine;
Heart;
Ischemia;
Myocardial Infarction;
Naloxone;
Purines;
Rats;
Receptors, Opioid;
Receptors, Purinergic P1;
Reperfusion;
Reperfusion Injury;
Tetrazolium Salts;
Theophylline;
Triazines;
Triazoles;
Xanthines
- From:Korean Journal of Anesthesiology
2012;63(4):340-345
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: The activation of guanine nucleotide binding protein-coupled receptors, such as adenosine receptor (ADR) and opioid receptor (OPR), protects the heart against ischemia and reperfusion injury. We hypothesized that ADR or OPR might be involved in polyphenol (-)-epigallocatechin gallate (EGCG)-induced cardioprotection. METHODS: Langendorff perfused rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Hearts were treated with 10 microM of EGCG, with or without the ADR or OPR antagonist at early reperfusion. Infarct size measured with 2,3,5-triphenyltetrazolium chloride staining was chosen as end-point. RESULTS: EGCG significantly reduced infarct volume as a percentage of ischemic volume (33.5 +/- 4.1%) compared to control hearts (14.4 +/- 1.1%, P < 0.001). A nonspecific ADR antagonist 8-(p-sulfophenyl) theophylline hydrate (27.1 +/- 1.9%, P < 0.05 vs. EGCG) but not a nonspecific OPR antagonist naloxone (14.3 +/- 1.3%, P > 0.05 vs. EGCG) blocked the anti-infarct effect by EGCG. The infarct reducing effect of EGCG was significantly reversed by 200 nM of the A1 ADR antagonist DPCPX (25.9 +/- 1.1%, P < 0.05) and 15 nM of the A2B ADR antagonist MRS1706 (29.3 +/- 1.7%, P < 0.01) but not by 10 microM of the A2A ADR antagonist ZM241385 (23.9 +/- 1.9%. P > 0.05 vs. EGCG) and 100 nM of the A3 ADR antagonist MRS1334 (24.1 +/- 1.8%, P > 0.05). CONCLUSIONS: The infarct reducing effect of EGCG appears to involve activation of ADR, especially A1 and A2B ADR, but not OPR.
