Objective      To investigate the effect of aryl hydrocarbon receptor (AhR) activation on the intestinal barrier function after acute intestinal ischemia reperfusion (I/R) in a mouse model.        Methods      Eighteen 6-8-week-old C57B L/6 mice were divided into 3 groups randomly

with 6 in each group: sham group

I/R group

and I/R+6-formylindolo(3

2-b)carbazole (FICZ) group. The mouse intestinal I/R model was established by mechanically blocking the superior mesenteric artery (SMA) temporarily for 30 min

following by reperfusion for 6 h. Histological changes in the small intestine were observed by hematoxylin-eosin staining (HE). The protein expression of AhR and tight junction protein ZO-1 in the intestine epithelium was detected by immunofluorescence assay and Western blotting.       Results      Both HE staining and immunofluorescence assay indicated the integrate intestinal villi with continuous ZO-1 expression on the surface of the villi alone in the sham group. The intestinal villi of the I/R group were partially dissociated

thickened

and fractured

meanwhile the destroyed continuity of ZO-1 turned up on the top of the villi. The intestinal villi of the I/R+FICZ group were neatly arranged and the damage to intestinal mucosa was alleviated obviously

with remarkable restoration of the continuity of ZO-1. Compared with the sham group

ZO-1 protein levels in the I/R group and the I/R + FICZ group were decreased by 50.7% and 32.3%

respectively (P0.05)

and compared with the I/R group

ZO-1 protein level in the I/R+FICZ group was increased by 37.2% (P0.05).        Conclusion      Pretreatment with FICZ can effectively alleviate the damage of intestinal mucosal structure and function in acute I/R model

and the possible mechanism is to increase the expression of ZO-1.