Role of JNK phosphorylation in intestinal ischemia/reperfusion injury in mice
10.3724/SP.J.1008.2010.00140
- Author:
De-Yi ZHENG
1
Author Information
1. Department of Burns
- Publication Type:Journal Article
- Keywords:
Apoptosis;
C-Jun NH2 terminal kinase;
Caspase-3;
Reperfusion injury;
Small intestine
- From:
Academic Journal of Second Military Medical University
2010;31(2):140-143
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the role of c-Jun NH2 terminal kinase (JNK) activation and JNK-mediated apoptotic signal pathway in intestinal ischemia/reperfusion (II/R) in mice. Methods: C57BL/6 mice were randomly divided into sham-operated group (n = 6) and II/R groups (n = 36); the latter was further divided according to time after perfusion (0,0. 5,1,4,6 and 12 h). Animal II/R model was established by clamping the superior mesenteric artery (SMA) for 40 min followed by reperfusion. Animals in the sham-operated group received no clamping. Animals in the two groups were sacrificed at defined time points, and the expression of JNK, phosphorylation (phospho-) JNK, cleaved caspase-3,Bcl-2 and Bax protein in the intestinal tissue was examined by Western blotting analysis, and the pathological changes of ileum tissue were observed under optical microscope. Results: Most severe intestinal injury was found at the early stage of reperfusion, and the intestinal tissues almost recovered 12 h later. The phospho-JNK in the intestine was significantly elevated within 1 h after II/R compared with sham group (P<0. 01). Cleaved caspase-3 was significantly increased in II/R group at 0. 5 h, 1 h after reperfusion compared to sham group (P<0. 01); the expression of Bcl-2 protein in II/R group was significantly decreased compared with the sham-operated group (P<0. 01), and there was no significant difference in Bax expression between different groups. Conclusion: JNK phosphorylation plays an essential role in the intestinal damages induced by II/R,possibly through down-regulating Bcl-2 protein expression and caspase-3 dependent apoptosis pathway.
