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
de En
| WPRIM
| ID: wpr-224612
Bibliothèque responsable:
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.
Mots clés
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Phosphorylation
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Reperfusion
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Technique de Western
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Récepteurs aux opioïdes
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2-(3,4-Dichlorophényl)-N-méthyl-N-((1S,2S)-2-(pyrrolidin-1-yl)cyclohexyl)acétamide
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Phosphatidylinositol 3-kinases
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Extracellular Signal-Regulated MAP Kinases
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Occlusion coronarienne
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Coeur
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Ischémie
Limites du sujet:
Animals
langue:
En
Texte intégral:
Korean Journal of Anesthesiology
Année:
2011
Type:
Article