Protective effect of parecoxib on intestinal barrier function of septic mice
- VernacularTitle:帕瑞昔布钠对脓毒症小鼠肠黏膜屏障的保护作用
- Author:
Youping WU
1
;
Jing YANG
;
Jie PENG
;
Wenbing XI
;
Weifeng TU
Author Information
1. 510010,广州军区广州总医院麻醉科
- Keywords:
Parecoxib;
Sepsis;
Intestinal barrier function;
Tight j unction protein
- From:
The Journal of Clinical Anesthesiology
2017;33(11):1091-1095
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of parecoxib on intestinal barrier function of septic mice.Methods Sepsis was induced by cecal ligation and puncture (CLP) model.Twenty-one male C57BL/6 mice were randomly divided into three groups (n =7 in each group):group Sham,group CLP,group P (parecoxib 2 mg/kg was administered via gastric tube 2 h after CLP).In vivo intestinal permeability was measured using an in vivo ligated loop model 24 h after surgery.Twenty-one male C57BL/6 mice were randomly divided into three groups as before.The small intestine tissue sample was harvested 24 h after surgery.The intestinal pathological changes were observed under light microscope.The expression of tight junction proteins ZO-1,Occludin,and Claudin-1 in the ileum were measured by Western blot.IL-6 and PGE2 level in the ileum were measured by ELISA.Results Compared with group Sham,the intestinal permeability was significantly increased and there was a significant intestinal pathological injury in group CLP.IL-6 and PGE2 level in the ileum was sig nificantly increased and the expression of tight junction protein ZO-1,Occludin,and Claudin-1 in the ileum were reduced in the group CLP (P＜0.05).Compared with the group CLP,intestinal permeability and pathological injury was significantly reduced in the group P.The levels of IL-6 and PGE2 were significantly decreased (P＜0.05),the expression of ZO-1,Occludin,and Claudin 1 were upregulated in group P (P＜0.05).Conclusion Parecoxib can decrease the levels of proinflammatory factors and up-regulate the expression of tight junction to reverse intestinal barrier dysfunction caused by sepsis in mice.
