JNK and p38 were involved in hypoxia and reoxygenation-induced apoptosis of cultured rat cerebellar granule neurons.
Exp Toxicol Pathol
; 61(2): 137-43, 2009 Mar.
Article
en En
| MEDLINE
| ID: mdl-18703324
As a model of the reperfusion injury found in stroke, we treated cerebellar granule neurons (CGNs) with hypoxia followed by reoxygenation. Hypoxia for 3h followed by 24h reoxygenation (H/R) induced a typical apoptosis of CGNs. CGNs exposed to H/R responded by activating JNK, increasing the expression of p38 and ultimately caused CGNs dying. Furthermore, apoptosis of CGNs induced by H/R was inhibited by pre-treatment with SB203580 or SP600125, and the inhibitory effect of SB203580 was greater than that of SP600125. Additionally, we also found that H/R temporally activated Akt and inactivated glycogen synthesis kinase-3beta (GSK-3beta), two proteins the functions of which were important in cell survival and energy metabolism. These findings demonstrated that H/R-induced apoptosis in CGNs by enhancing JNK and p38 activity, which contributed at least in part to H/R-induced apoptosis of CGNs.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Oxígeno
/
Cerebelo
/
Apoptosis
/
Proteínas Quinasas JNK Activadas por Mitógenos
/
Proteínas Quinasas p38 Activadas por Mitógenos
/
Neuronas
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Exp Toxicol Pathol
Asunto de la revista:
PATOLOGIA
/
TOXICOLOGIA
Año:
2009
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Alemania