Kappa-opioid receptor activation during reperfusion limits myocardial infarction via ERK1/2 activation in isolated rat hearts

June Hong KimYoung Ho JangKook Jin ChunJun KimYong Hyun ParkJeong Su KimJin Mo KimMi Young Lee
Dept. of Anesthesiology & Pain Medicine (마취통증의학); Dept. of Preventive Medicine (예방의학); Institute for Medical Science (의과학연구소)
Issue Date
Korean Journal of Anesthesiology, Vol.60(5) : 351-356, 2011
Background: We investigated whether p42/p44 extracellular signal-regulated kinases (ERK1/2) and/or phosphatidylinositol-3-OH kinase (PI3K)-Akt play a crucial role in cardioprotection by κ-opioid receptor (KOP) activation. Methods: Langendorff perfused rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Antagonists of ERK1/2 and PI3K were perfused in hearts treated with the KOP agonist U50488H (U50). Infarct size was measured after 2 h of reperfusion. The phosphorylation states of ERK1/2 and Akt by Western immunoblots were determined. Drugs were perfused for a period of 5 min before and 30 min after reperfusion. Results: Inhibition of ERK1/2 (26.8 ± 2.9%, P < 0.05 vs. U50) but not PI3K (15.5 ± 1.1%, P > 0.05 vs. U50) completely abrogated the anti-infarct effect of U50488H. Western blot analysis revealed a significant increase in ERK1/2 but not Akt phsophorylation in U50488H-treated hearts as compared to control hearts when measured immediately after reperfusion. Conclusions: KOP activation effectively reduces myocardial infarction. The anti-infarct effect of U50488H is mediated by the ERK1/2, but not the PI3K-Akt pathway.
Coronary occlusionHeartMyocardial functionOpioid receptorsReperfusion
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1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Anesthesiology & Pain Medicine (마취통증의학)
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Preventive Medicine (예방의학)
1. Journal Papers (연구논문) > 3. Research Institutues (연구소) > Institute for Medical Science (의과학연구소)
Keimyung Author(s)
김진모; 이미영
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