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.
Artigo
em Inglês
| WPRIM
| ID: wpr-224612
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fosforilação
/
Reperfusão
/
Western Blotting
/
Receptores Opioides
/
(trans)-Isômero de 3,4-dicloro-N-metil-N-(2-(1-pirrolidinil)-ciclo-hexil)-benzenoacetamida
/
Fosfatidilinositol 3-Quinases
/
MAP Quinases Reguladas por Sinal Extracelular
/
Oclusão Coronária
/
Coração
/
Isquemia
Limite:
Animais
Idioma:
Inglês
Revista:
Korean Journal of Anesthesiology
Ano de publicação:
2011
Tipo de documento:
Artigo
Similares
MEDLINE
...
LILACS
LIS