Activation of c-Jun N-terminal kinase 1/2 regulated by nitric oxide is associated with neuronal survival in hippocampal neurons in a rat model of ischemia / 中华医学杂志(英文版)
Chinese Medical Journal
; (24): 3367-3372, 2011.
Article
em En
| WPRIM
| ID: wpr-319115
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WPRO
ABSTRACT
<p><b>BACKGROUND</b>C-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in cerebral ischemia. Although the mechanistic basis for this activation of JNK1/2 is uncertain, oxidative stress may play a role. The purpose of this study was to investigate whether the activation of JNK1/2 is associated with the production of endogenous nitric oxide (NO).</p><p><b>METHODS</b>Ischemia and reperfusion (I/R) was induced by cerebral four-vessel occlusion. Sprague-Dawley (SD) rats were divided into 6 groups: sham group, I/R group, neuronal nitric oxide synthase (nNOS) inhibitor (7-nitroindazole, 7-NI) given group, inducible nitric oxide synthase (iNOS) inhibitor (2-amino-5,6-dihydro-methylthiazine, AMT) given group, sodium chloride control group, and 1% dimethyl sulfoxide (DMSO) control group. The levels of protein expression and phospho-JNK1/2 were detected by Western blotting and the survival hippocampus neurons in CA1 zone were observed by cresyl violet staining.</p><p><b>RESULTS</b>The study illustrated two peaks of JNK1/2 activation occurred at 30 minutes and 3 days during reperfusion. 7-NI inhibited JNK1/2 activation during the early reperfusion, whereas AMT preferably attenuated JNK1/2 activation during the later reperfusion. Administration of 7-NI and AMT can decrease I/R-induced neuronal loss in hippocampal CA1 region.</p><p><b>CONCLUSION</b>JNK1/2 activation is associated with endogenous NO in response to ischemic insult.</p>
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Assunto principal:
Farmacologia
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Fosforilação
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Isquemia Encefálica
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Western Blotting
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Ratos Sprague-Dawley
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Biologia Celular
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Proteína Quinase 8 Ativada por Mitógeno
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Proteína Quinase 9 Ativada por Mitógeno
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Inibidores Enzimáticos
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Óxido Nítrico Sintase Tipo II
Limite:
Animals
Idioma:
En
Revista:
Chinese Medical Journal
Ano de publicação:
2011
Tipo de documento:
Article