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.
Conclusions
The infarct reducing effect of EGCG appears to involve activation of ADR, especially A(1) and A(2B) ADR, but not OPR.
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 A(1) ADR antagonist DPCPX (25.9 ± 1.1%, P < 0.05) and 15 nM of the A(2B) ADR antagonist MRS1706 (29.3 ± 1.7%, P < 0.01) but not by 10 µM of the A(2A) ADR antagonist ZM241385 (23.9 ± 1.9%. P > 0.05 vs. EGCG) and 100 nM of the A(3) ADR antagonist MRS1334 (24.1 ± 1.8%, P > 0.05). Conclusions: The infarct reducing effect of EGCG appears to involve activation of ADR, especially A(1) and A(2B) ADR, but not OPR.