RESUMO
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.
RESUMO
Objective To investigate the change of high mobility group box 1 ( HMGBI ) after intestine ischemia reperfusion (I/R) in rats, compare the effect of drainage of intestine lymph fluid on gut barrier, and ex- plore the possible mechanism of iachemia-reporfusion injury. Methods Thirty-two Sprague-Dawley (SD) rats (SPF grade) were randomly divided into4 groups with 8 rats in each group: blank group, sham group, intestine is-chemia-reperfusion (I/R) group, and intestine ischemia-reperfusion with drainage of intestine lymph fluid (I/R +drainage) group. Indicators of gut barrier function damage, translocation of endotoxin, and change of HMGB1 and cytokines were detected after intestine ischemia-reperfusion injury. Results The gut barrier function damage and levels of endotoxin, HMGBI, tumour necrosis factor-alpha ( TNF-α), interleukin-6 ( IL-6 ), interleukin-1 beta (IL-1β), and soluble intercellular adhesion molecule-1 (sICAM-1) were significantly lower in blank group and sham group than in I/R group and I/R + drainage group ( P < 0. 05 ). Compared with the intestine I/R + drainage group, the levels of endotoxin and cytokines were significantly higher in the intestine I/R group. The level of HMGB1 was slightly higher than that in the intestine I/R + drainage group, but such difference was not statistically significant ( P > 0. 05 ). lmmunohistochemical staining also revealed that the expression of HMGB1 was significant- ly higher in I/R group than in I/R + drainage group. Conclusions Intestine iachemia-reperfusion injury can lead to the injury of intestine mucosal barrier and increase HMGB1 level HMGB1 may deteriorate gut barrier function and increase the leveh of systemic cytokines. Drainage of lymph fluid can block the gut-lymph pathway and thus decrease the levels of endotoxin and cytokines in systemic circulation and attenuate intestine ischemia-reperfusion injury.