Effects of extracellular signal-regulated kinase (ERK) on focal cerebral ischemia / 中华医学杂志(英文版)
Chinese Medical Journal
;
(24): 1497-1503, 2003.
Artigo
em Inglês
| WPRIM
| ID: wpr-311648
ABSTRACT
<p><b>OBJECTIVE</b>To determine the role of extracellular signal-regulated kinase (ERK)1/2 during focal cerebral ischemia.</p><p><b>METHODS</b>Left middle cerebral artery occlusion (MCAO) was undergone after the introduction of a nylon suture to the left internal carotid artery in 70 male adult CD-1 mice. ERK 1/2 phosphorylation was detected using Western blot analysis, and the morphological feature was determined by immunohistochemistry. An ERK pathway inhibitor, 1,4-diamino-2,3-dicyano-1,4-bis[2-amino-phenylthio] butadiene (U0126), was administered intravenously 20 minutes before MCAO, and the neurological deficit levels and the infarct volumes were measured 24 hours after MCAO.</p><p><b>RESULTS</b>Phosphorylated ERK 1/2 (pERK 1/2) activity increased after 30 minutes of MCAO and peaked at 2 hours. The immunohistochemical study displayed a large number of pERK 1/2 positive cells in the ischemic basal ganglion and surrounding cortex. Double-labeled fluorescent staining identified the pERK1/2 positive cells as neurons or astrocytes. In U0126 treated mice which had undergone 24 hours of MCAO, the neurological deficit levels and the infarct volumes were 44.6% and 45.8% respectively, less than those of the control mice.</p><p><b>CONCLUSIONS</b>ERK plays an important role in focal cerebral ischemia and inhibition of the ERK pathway can help protect against ischemic brain injury, which may provide a therapeutic approach for cerebral ischemia.</p>
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Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Farmacologia
/
Fosforilação
/
Fisiologia
/
Gânglios da Base
/
Butadienos
/
Imuno-Histoquímica
/
Córtex Cerebral
/
Isquemia Encefálica
/
Proteínas Quinases Ativadas por Mitógeno
Limite:
Animais
Idioma:
Inglês
Revista:
Chinese Medical Journal
Ano de publicação:
2003
Tipo de documento:
Artigo
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