期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 704, 期 1-3, 页码 64-69出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2013.02.010
关键词
Enterobacteria; Lactobacillales; Bacteroides; Clostridium; Terminal restriction fragment length polymorphism
资金
- Grants-in-Aid for Scientific Research [23590924] Funding Source: KAKEN
Enterobacteria play important roles in the pathophysiology of small intestinal injuries induced by nonsteroidal anti-inflammatory drugs (NSAIDs). We investigated the effects of rebamipide, a gastrointestinal mucoprotective drug, on indomethacin-induced small intestinal injuries, intestinal microbiota, and expression levels of alpha-defensin 5, which is a Paneth cell-specific antimicrobial peptide and is important for the regulation of intestinal microbiota. Indomethacin (10 mg/kg) was orally administered to mice after oral administration of rebamipide (100 or 300 mg/kg) or vehicle for 1 week, and the small intestinal injuries were assessed. After oral administration of rebamipide, the small intestinal contents were subjected to terminal restriction fragment length polymorphism (T-RFLP) analysis to assess the intestinal microbiota composition. Further, the expression levels of mRNA and protein for alpha-defensin 5 in the ileal tissue were determined by real-time reverse transcription-polymerase chain reaction and western blotting analysis, respectively. Rebamipide inhibited indomethacin-induced small intestinal injuries and T-RFLP analysis showed that rebamipide increased the percentage of Lactobacillales and decreased the percentage of Bacteroides and Clostridium than that in vehicle-treated controls. The mice that were treated with rebamipide showed an increase in alpha-defensin 5 mRNA expression and protein levels in the ileal tissue compared to vehicle-treated control mice. Indomethacin reduced expression of alpha-defensin 5 mRNA in ileal tissue, while rebamipide reversed expression of alpha-defensin 5 mRNA. In conclusion, our study results suggest that rebamipide inhibits indomethacin-induced small intestinal injuries, possibly by modulating microbiota in the small intestine by upregulation of alpha-defensin 5. (C) 2013 Elsevier BY. All rights reserved.
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