Hypoxia-reoxygenation differentially stimulates stress-activated protein kinases in primary-cultured rat hepatocytes.
Transpl Int
; 13 Suppl 1: S597-9, 2000.
Article
en En
| MEDLINE
| ID: mdl-11112081
ABSTRACT
Organ injury after ischemia and reperfusion (I/R) remains one of the most important limiting factors in liver surgery and transplantation. Oxygen-free radical (OFR) generation is considered a major cause of this damage. JNK1/SAPK1, a member of MAPK family, regulates cell adaptation to stressful conditions. The aim of this study was to determine if hypoxia-reoxygenation (H/R) can activate JNK1/SAPK1 and if OFR are involved in this activation. Primary cultured rat hepatocytes isolated from other liver cells and blood flow were submitted to warm and cold H/R phases mimicking surgical and transplant conditions. JNK1/SAPK1 was activated by both warm and cold H/R. Deferoxamine (1 mM), di-phenyleneiodonium (50 microM) and N-acetylcysteine (10 mM) significantly inhibited this kinase activation.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Hipoxia de la Célula
/
Estrés Oxidativo
/
Proteínas Quinasas Activadas por Mitógenos
/
Hepatocitos
Límite:
Animals
Idioma:
En
Revista:
Transpl Int
Asunto de la revista:
TRANSPLANTE
Año:
2000
Tipo del documento:
Article
País de afiliación:
Francia