Rebamipide repairs injury of small intestinal epithelial barrier induced by aspirin in mice
10.3969/j.issn.1000-4718.2017.09.022
- VernacularTitle:瑞巴派特对阿司匹林诱导的小鼠小肠上皮屏障损伤的修复
- Author:
Liu SHI
1
;
sheng Zhong XIA
;
Yu LAI
;
yi Si WANG
;
ting Wen BI
;
Yu LIU
;
Tao YU
;
kui Qi CHEN
Author Information
1. 赣州市人民医院消化内科
- Keywords:
Rebamipide;
Aspirin;
Small intestinal injury;
β-catenin;
Cyclooxygenase-2
- From:
Chinese Journal of Pathophysiology
2017;33(9):1669-1675
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate whether rebamipide repairs the small intestinal epithelial barrier in aspirin-induced small intestinal injury (SII) in mice and its mechanism.METHODS:Small intestinal injury was induced by aspirin (200 mg · kg-1 · d-1 for 5 d) in BALB/c mice.Based on the treatment with aspirin and/or rebamipide (320 mg ·kg-1 · d-1),the mice were divided into 4 groups (n =18 in each group).The living mice in each group (n =6) were sacrificed via cervical dislocation method at day 0,day 5,and day 10.The structure and function of intestinal barrier and the levels of the signaling pathway factors were measured by transmission electron microscopy,immunohistochemistry,qPCR,and Western blot.RESULTS:Tight junctions between intestinal epithelial cells improved significantly after rebamipide treatment.The expression of ZO-1 and occludin in the injured small intestine showed a gradually increasing trend after rebamipide administration (P < 0.05).There was a decreased trend of D-lactate level in rebamipide-treated SII mice (P < 0.05).The expression of cyolooxygenase-2 (COX-2),β-catenin,and c-Myc,and prostaglandin E2 concentration in small intestinal tissues were significantly increased in rebamipide treatment group (P < 0.05).However,down-regulated COX-1 expression in the SII mice was sustained at a low level after rebamipide administration.CONCLUSION:Rebamipide repairs the injury of small intestinal mucosa and improves the structure and function of small intestinal barrier in aspirininduced SII mice by up-regulating the expression of COX-2.