Up-regulation of iNOS by hypoxic postconditioning inhibits H9c2 cardiomyocyte apoptosis induced by hypoxia/re-oxygenation.
Acta Biochim Biophys Sin (Shanghai)
; 47(7): 516-21, 2015 Jul.
Article
em En
| MEDLINE
| ID: mdl-26040314
ABSTRACT
Apoptosis is a crucial mode of cell death induced by ischemia and reperfusion, and ischemic postconditioning (PostC) has been reported to inhibit cell apoptosis. Inducible nitric oxide synthase (iNOS) has been confirmed to play an important role in triggering and mediating the late cardio-protection against ischemia/hypoxia. In this study, we found that hypoxic PostC remarkably up-regulated the expression of iNOS and decreased cardiomyocyte apoptosis. Pre-treatment with 1400w (a highly selective inhibitor of iNOS) or iNOS siRNA weakened the anti-apoptotic effect of hypoxic PostC. These findings suggested that iNOS may be one of the key molecular mechanisms responsible for the inhibition of apoptosis by hypoxic PostC.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Regulação para Cima
/
Miócitos Cardíacos
/
Óxido Nítrico Sintase Tipo II
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Pós-Condicionamento Isquêmico
Limite:
Animals
Idioma:
En
Revista:
Acta Biochim Biophys Sin (Shanghai)
Ano de publicação:
2015
Tipo de documento:
Article