Experimental Research Article Korean J Anesthesiol 2012 October 63(4): 340-345 http://dx.doi.org/10.4097/kjae.2012.63.4.340 Polyphenol (-)-epigallocatechin gallate-induced cardioprotection may attenuate ischemia-reperfusion injury through adenosine receptor activation: a preliminary study Sang Kwon Lee1, June Hong Kim2, Jeong Su Kim2, Youngho Jang2, Jun Kim2, Yong Hyun Park2, Kook Jin Chun2, and Mi Young Lee3 1Department of Thoracic and Cardiovascular Surgery, 2Institute of Cardiovascular Research Center, Pusan National University Yangsan Hospital, Yangsan, and 3Department of Preventive Medicine, Keimyung University School of Medicine, Daegu, Korea 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 μM 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 μM 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. (Korean J Anesthesiol 2012; 63: 340-345) Key Words: Adenosine, Epigallocatechin gallate, Myocardial infarction, Reperfusion injury. Received: June 14, 2012. Revised: July 12, 2012. Accepted: August 6, 2012. Corresponding author: Youngho Jang, M.D., Ph.D., Institute of Cardiovascular Research Center, Pusan National University Yangsan Hospital, Beomeo-ri, Mulgeum-eup, Yangsan 626-770, Korea. Tel: 82-53-471-2800, Fax: 82-53-471-2806, E-mail: weonjo@pnuyh.co.kr CC This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http:// creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright ⓒ the Korean Society of Anesthesiologists, 2012 www.ekja.org