Expressions of the pERK1/2 and the cFos Proteins at an Early Stage of Transient Global Ischemia-reperfusion Injury in the Hippocampus of Rats
Journal of the Korean Society of Emergency Medicine
;
: 475-486, 2004.
Artículo
en Coreano
| WPRIM
| ID: wpr-104408
ABSTRACT
PURPOSE:
This study was to evaluate temporal changes in the expressions of the phosphorylated extracellular-regulated kinase1/2 (pERK1/2), the phosphorylated MAPK/ERK kinase1/2 (pMEK1/2) and the cFos proteins in the hippocampus of rats following transient global ischemia.METHODS:
Transient global ischemia was induced in the forebrains of Sprague-Dawley rats by using a 4-vessel occlusion for 20 min under anesthetic condition. Hematoxyline-eosin staining showed typical microscopic findings that represented neuronal cell death in hippocampal CA1 regions 5 days after transient global ischemia. Four-vessel occlusion-reperfusion produced ischemic injury in major forebrain structures, such as the striatum, the cortex and the hippocampus, in the finding of triphenyltetrazolium chloride (TTC) staining.RESULTS:
A high density of pERK1/2 immunoreactivity existed in the pyramidal-cell layers of the CA2-3 regions and in the granular-cell layers of the dentate gyrus 5 min after ischemia. Following ischemia, expression of the pMEK1/2 protein showed temporal changes similar to that of the pERK1/2 protein. A significant expression of the cFos protein was noted in the pyramidal-cell layers of the CA2-3 regions and in the granular-cell layers of the dentate gyrus 2 hours after global ischemia.CONCLUSION:
Intracellular signaling cascades of the ERK or the cFos protein take part in early cellular events in the hippocampus of rats in response to ischemic insult.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Daño por Reperfusión
/
Prosencéfalo
/
Muerte Celular
/
Ratas Sprague-Dawley
/
Giro Dentado
/
Región CA1 Hipocampal
/
Hipocampo
/
Isquemia
/
Neuronas
Límite:
Animales
Idioma:
Coreano
Revista:
Journal of the Korean Society of Emergency Medicine
Año:
2004
Tipo del documento:
Artículo
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