Role of p38 MAPK signaling in lung injury following intestinal ischemia/reperfusion in mice
10.3724/SP.J.1008.2010.00254
- Author:
De-Yi ZHENG
1
Author Information
1. Department of Burns
- Publication Type:Journal Article
- Keywords:
Intestinal;
Lung injury;
P38 mitogen-activated protein kinase;
Reperfusion injury;
SB239063
- From:
Academic Journal of Second Military Medical University
2010;31(3):254-257
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the possible role of p38 mitogen-activated protein kinase (MAPK) in lung injury following intestinal ischemia reperfusion (II/R) in mice. Methods Intestinal ischemia/reperfusion was induced by occluding the superior mesenteric artery for 45 min followed by 6 h reperfusion. C57BL/6 mice were randomly divided into sham-operated group (sham group), II/R group and II/R plus SB239063 treatment (SB239063 group), n = 6/group. SB239063 (3 mg/kg), a novel second-generation p38 MAPK inhibitor, was administered intraperitoneally one hour before clamping. Pulmonary p38 MAPK and phospho-p38 MAPK protein were measured by Western blotting analysis. Gene expression of TNF-α and IL-1β in the lung was analyzed by RT-PCR. The lung pathology was observed by optical microscope. Results Compared with the sham- operated group, pulmonary p38 MAPK activation was significantly increased 6 h after II/R (P<0. 01), whereas SB239063 could markedly attenuate p38 MAPK activation in lung tissue (P<0. 05). In addition, the increased TNF-α and IL-1β mRNA levels induced by II/R in lungs were significantly blocked by inhibiting p38 MAPK activation (P<0. 05). SB239063 treatment ameliorated the pathologic lung injury induced by II/R. Conclusion p38 MAPK plays an important role in lung injury induced by intestinal ischemia reperfusion (II/R) in mice, and inhibition of p38 MAPK activation prevents lung injury following II/R in mice.
