Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Añadir filtros








Intervalo de año
1.
Korean Journal of Pathology ; : 364-371, 2004.
Artículo en Inglés | WPRIM | ID: wpr-112683

RESUMEN

BACKGROUND: Neuronal death in acute-phase cerebral ischemic injury is caused by necrosis. However, neuronal injury after reperfusion can be associated with apoptosis. METHODS: We used Sprague-Dawley rats whose brains were reperfused after middle cerebral artery occlusion for either 30 min or 2 h. We examined a relationship between apoptosis and the expression of inducible nitric oxide synthase (iNOS) in the brain tissue from 3 h to 14 days after reperfusion in both groups. RESULTS: TUNEL and iNOS positivity were closely related in both groups. The 2-h ischemia group exhibited increases in the amount of TUNEL and iNOS-positive cells for up to 3 days after reperfusion, at which the TUNEL and iNOS-positive cells decreased. The 30-min ischemia group exhibited peak positivity 24 h after reperfusion, followed by a similar decrease. iNOS mRNA expression peaked 3 h after reperfusion in the 30-min ischemia group, at which time it decreased. In the 2-h ischemia group, iNOS mRNA increased 3 h after reperfusion, peaked 24 h after reperfusion, and then decreased. CONCLUSION: These results indicated the occurrence of delayed apoptosis in transient cerebral ischemia. Increased expression of iNOS is closely associated with this apoptosis, and oxygen free radical-producing materials, such as nitric oxide, may play an important role in the induction of this apoptosis.


Asunto(s)
Apoptosis , Encéfalo , Isquemia Encefálica , Etiquetado Corte-Fin in Situ , Infarto de la Arteria Cerebral Media , Isquemia , Ataque Isquémico Transitorio , Necrosis , Neuronas , Óxido Nítrico , Óxido Nítrico Sintasa de Tipo II , Oxígeno , Ratas Sprague-Dawley , Reperfusión , ARN Mensajero
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA