PI3K-Akt/eNOS in remote postconditioning induced by brief pulmonary ischemia.
Clin Invest Med
; 37(1): E26-37, 2014 Feb 01.
Article
en En
| MEDLINE
| ID: mdl-24502809
ABSTRACT
PURPOSE:
Postconditioning, a series of brief ischemia-reperfusion sequences given before an ischemic heart undergoes sustained reperfusion, has been shown to lessen ischemia/reperfusion injury. The current study establishes a rabbit model of myocardial ischemia-reperfusion and studied the effects of pulmonary remote postconditioning in this model.METHODS:
Serum levels of creatine kinase (CK), superoxide dismutase (SOD), and malondialdehyde (MDA), protein expression of endothelial nitric oxide synthase (eNOS), Rho kinase (ROCK- 2), and protein kinase B (Akt) in myocardial cells and the apoptosis index of myocardial cells were examined.RESULTS:
Pulmonary remote postconditioning decreased CK, significantly decreased MDA, and increased SOD. Postconditioning significantly increased eNOS protein expression. Administration of eNOS inhibitor, L-NAME, dramatically suppressed the postconditioning-induced eNOS protein expression and serum SOD level, but significantly increased MDA level. The two longer sessions of postconditioning increased Akt, although this increase was not accompanied by changes in levels of the Akt inhibitor, ROCK-2. Blocking eNOS activity with L-NAME had no visible effect on either Akt or ROCK-2.CONCLUSION:
Our results suggest a role for Akt in remote postconditioning-induced myocardial protection, but do not support an involvement of eNOS in Akt-mediated action.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Daño por Reperfusión Miocárdica
/
Precondicionamiento Isquémico
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Fosfatidilinositol 3-Quinasas
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Óxido Nítrico Sintasa de Tipo III
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Proteínas Proto-Oncogénicas c-akt
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Pulmón
Límite:
Animals
Idioma:
En
Revista:
Clin Invest Med
Año:
2014
Tipo del documento:
Article