Polyphenol (-)-epigallocatechin gallate-induced cardioprotection may attenuate ischemia-reperfusion injury through adenosine receptor activation: a preliminary study

다국어 초록 (Multilingual 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 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.

다국어 초록 (Multilingual 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 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.

참고문헌 (Reference)

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