Kappa-opioid receptor activation during reperfusion limits myocardial infarction via ERK1/2 activation in isolated rat hearts / 대한마취과학회지
Korean Journal of Anesthesiology
; : 351-356, 2011.
Article
in En
| WPRIM
| ID: wpr-224612
Responsible library:
WPRO
ABSTRACT
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 kappa-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) 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.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Phosphorylation
/
Reperfusion
/
Blotting, Western
/
Receptors, Opioid
/
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
/
Phosphatidylinositol 3-Kinases
/
Extracellular Signal-Regulated MAP Kinases
/
Coronary Occlusion
/
Heart
/
Ischemia
Limits:
Animals
Language:
En
Journal:
Korean Journal of Anesthesiology
Year:
2011
Type:
Article