Interleukin-1beta expression and phospholipase A(2) activation after intestinal ischemia/reperfusion injury.
Sheng Li Xue Bao
; 54(1): 28-32, 2002 Feb 25.
Article
en En
| MEDLINE
| ID: mdl-11930237
ABSTRACT
The experiments were carried out to explore the interactions between IL-1 beta gene expression, protein level and phospholipase A(2) PLA(2) inhibition after intestinal ischemia/reperfusion injury. Using a rat intestinal ischemia/reperfusion injury model, after collecting the serum, lung lavage, abdomen cavity lavage and important organ tissue samples from control, injury and PLA(2) inhibitor treated groups, IL-1 beta level was measured by radioimmunoassay, and the mRNA expression of IL-1 beta and type II PLA (2)was determined by RT-PCR. After 6 h of injury, the IL-1 beta level in serum was significantly higher than that in the control group; an increase in IL-1 beta was also observed in abdomen cavity lavage 1 or 3 h after injury. IL-1 beta was significantly increased in liver tissue after injury, but was not changed obviously in the lung, kidney and intestinal tissues. IL-1 beta in the lung lavage was significantly higher than that of control group. The mRNA expression of IL-1 beta in lung tissue was increased after injury, but type II PLA(2) mRNA expression was decreased. There were different changes in IL-1 beta level and gene expression after treatment with PLA(2) inhibitor chloroquine, cyclo-oxidase inhibitor indomethacin, or PAF receptor antagonist SR27417 respectively after injury. All these results indicate that after intestinal ischemia/reperfusion injury, the IL-1 beta level and mRNA gene expression are significantly increased, however, the relationship among IL-1 beta, PLA(2) activation and its metabolite release remains to be further elucidated.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Fosfolipasas A
/
Daño por Reperfusión
/
Interleucina-1
/
Intestinos
/
Isquemia
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Sheng Li Xue Bao
Año:
2002
Tipo del documento:
Article