ABSTRACT
Objective To investigate the effect and mechanism of epigallocatechin-3-gallate(EGCG) on intestine ischemia reperfusion injury(IRI) in rats. Methods Forty SD rats were randomly and equally divided into 4 groups:sham group(Sham),intestinal ischemia reperfusion injury group(IRI),EGCG pretreatment group(EGCG) and HLY78 group (Wnt-Ag).The IRI,EGCG and WNT-AG groups were performed the superior mesenteric artery(SMA) ligation for 45 min by non-injury vascular clamp to construct the IRI model.EGCG (50 mg/kg) was administrated by intraperitoneal injection at 45 min before ischemia in EGCG group.The Wnt-Ag group was administrated by intraperitoneal injection of EGCG(50 mg/kg) plus Wnt-Ag (5 mg/kg) at 45 min before ischemia.The IRI group and Sham group were administrated by same dosage of normal saline.The pathological morphology of intestinal tissue was observed by staining at 4 h after reperfusion.The cellular apoptosis was detected by immunohistochemistry.The expressions of tumor necrosis factor-α(TNF-α),interleukin-1(IL-1),interleukin-6(IL-6) in the serum and intestinal tract were examined by ELISA and RT-PCR.The expressions of Wnt,β-catenin,p53,Bax and BCL-2 were measured by Western blot.Results Compared with the Sham group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,Bax,cell apoptosis and pathological change of intestinal tract in the IRI group were significantly increased,while the expression of BCL-2 was significantly decreased.Compared with the IRI group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,p53,Bax,cell apoptosis and the pathological change of intestinal tracrt in the EGCG group were significantly decreased,while the expression of BCL-2 was significantly increased.Compared with the EGCG group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,Bax,cell apoptosis and pathological change of intestinal tract in the Wnt-Ag group were increased,while the expression of BCL-2 was significantly decreased.Conclusion EGCG can alleviate intestine ischemia-reperfusion injury by suppressing inflammation and apoptosis,this protective effect may be mediated by suppressing Wnt/β-catenin signal pathway.