Rosiglitazone Pretreatment Ameliorates Intestinal Ischemia-reperfusion Injury
10.3969/j.issn.1008-7125.2014.08.006
- VernacularTitle:罗格列酮预处理能减轻小肠缺血再灌注损伤
- Author:
Wei YUAN
;
Hui LIU
;
Meixue CHEN
;
Liping PAN
- Publication Type:Journal Article
- Keywords:
Rosiglitazone;
PPAR gamma;
Reperfusion Injury;
Cytokines
- From:
Chinese Journal of Gastroenterology
2014;(8):472-475
- CountryChina
- Language:Chinese
-
Abstract:
Background:Intestinal ischemia-reperfusion( I/R)is a surgical abdomen,which not only leads to intestinal tissue necrosis,but also induces systemic inflammatory response,resulting in a serious impact on other organs and tissues. Aims:To investigate the role and mechanism of rosiglitazone( ROS)on intestinal I/R injury. Methods:Eighteen male C57BL/6 mice were randomly divided into three groups:sham operation group,I/R injury group and ROS pretreatment group. Mice in ROS pretreatment group received ROS(0. 3 mg/kg,IV)30 minutes before I/R injury. I/R injury model was established by clamping superior mesenteric artery for 30 minutes,followed by 4 hours reperfusion. All the mice were sacrificed. The pathology of intestinal tissue was examined by HE staining. The mRNA expressions of tumor necrosis factor( TNF )-α, interferon(IFN)-γ,interleukin( IL)-1β,transforming growth factor( TGF)-β and Smad3 were measured by real-time quantitative PCR. The protein expressions of TGF-βand Smad3 were measured by Western blotting. Serum levels of TNF-α, IFN-γand IL-1βwere measured by ELISA. Results:Compared with the sham operation group,pathological score of small intestinal mucosa in I/R injury group was significantly increased(P<0. 05),and the mRNA expressions of TNF-α,IFN-γand IL-1β were significantly increased( P < 0. 05 ),the mRNA and protein expressions of TGF-β and Smad3 were significantly increased(P<0. 05),the serum levels of TNF-α,IFN-γand IL-1β were significantly increased(P<0. 05). With the pretreatment of ROS,all the above-mentioned indices were significantly ameliorated(P<0. 05). Conclusions:ROS pretreatment can attenuate intestinal I/R injury by inhibiting TGF-β/Smad3 signal pathway to reduce inflammation.
