Pretreatment with Dexamethasone Ameliorates Intestinal Ischemia Reperfusion Injury
10.3870/yydb.2015.05.003
- VernacularTitle:地塞米松预处理减轻小肠缺血-再灌注损伤
- Author:
Wei YUAN
;
Juan YANG
;
Meixue CHEN
;
Liping PAN
- Publication Type:Journal Article
- Keywords:
Dexamethasone;
Injury,ischemia reperfusion,intestine;
Inflammation
- From:
Herald of Medicine
2015;(5):574-577
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate potential effect and mechanism of dexamethasone ( DEX) on intestinal ischemia reperfusion injury. Methods A total of 18 male C57BL/6 mice were randomly divided into three groups( n=6 each): sham operation group, model control group , and DEX group. Mice in the model control and sham operation groups received intraperitoneal normal saline 0. 5 hour before ischemia, and mice in DEX group received intraperitoneal injection of DEX 10 mg·kg-1 , 0. 5 hour before ischemia. Mice in the model control and DEX groups were placed in the 32 degree infant incubator for 30 minutes after clamping superior mesenteric artery, followed by clamps removal and reperfusion for 24 hours. Mice were then sacrificed to obtain the intestinal tissues. The pathology of intestinal tissues was observed after hematoxylin-eosinstaining ( HE) staining. The mRNA expression level of pro-inflammatory cytokines IL-6, TNF-α and IFN-γ were measured by PCR. The expression of AKT and p-AKT were measured by Western blotting. Results The level of mesenteric injuries in the sham operation group, model control group and DEX group was (4±2),(13±3),(7±2) points, respectively. The mRNA level of IL-6, TNF-α and IFN-γ and the expression of p-AKT were all higher in the model control group. Compared to the model control group, the level of mesenteric injuries, the mRNA level of IL-6, TNF-αand IFN-γin DEX group were significantly attenuated, but the expression of p-AKT were further increased. Conclusion Pretreatment with DEX can reduce intestinal ischemia-reperfusion injury by activating AKT signaling pathway and suppressing inflammation.
