SP600125, a selective JNK inhibitor, aggravates hepatic ischemia-reperfusion injury
Experimental & Molecular Medicine
;
: 408-416, 2006.
Artículo
en Inglés
| WPRIM
| ID: wpr-53149
ABSTRACT
c-Jun N-terminal kinase (JNK) is activated during hepatic reperfusion, and JNK inhibitors are known to protect other major organs from ischemia-reperfusion (I/R) injury. We attempted to determine the effect of SP600125, a JNK inhibitor, on hepatic I/R injury using a partial ischemia model in mice. Compared to a vehicle-treated group, the SP600125-treated group showed a greater increase in serum ALT levels 24 h after reperfusion with more severe parenchymal destruction and leukocyte infiltration. Similarly, tissue myeloperoxidase and malondialdehyde levels were higher in the SP600125-treated group, and chemokine expression was also higher in the SP600125-treated group. These data, which are contradictory to previous results, indicate that JNK inhibition by SP600125 may be harmful in hepatic I/R injury. Therefore, care must be taken when investigating the therapeutic use of JNK inhibitors in hepatic I/R injury, especially in the context of the effects of JNK inhibition on inflammatory infiltration.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Daño por Reperfusión
/
Estrés Oxidativo
/
Quimiocinas
/
Metaloproteinasa 9 de la Matriz
/
MAP Quinasa Quinasa 4
/
Hígado
/
Antracenos
/
Ratones Endogámicos C57BL
Límite:
Animales
Idioma:
Inglés
Revista:
Experimental & Molecular Medicine
Año:
2006
Tipo del documento:
Artículo
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