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. 2009:44 Suppl 19:35-9.
doi: 10.1007/s00535-008-2267-5. Epub 2009 Jan 16.

Mast cells are involved in the pathogenesis of indomethacin-induced rat enteritis

Tetsuya Okayama  1 , Norimasa Yoshida, Kazuhiko Uchiyama, Tomohisa Takagi, Hiroshi Ichikawa, Toshikazu Yoshikawa
Affiliations

Mast cells are involved in the pathogenesis of indomethacin-induced rat enteritis

Tetsuya Okayama et al. J Gastroenterol. 2009.

Abstract

Background: Nonsteroidal antiinflammatory drug (NSAID)-induced enteropathy is clinically very important, but the pathological mechanisms remain unclear. Mast cells have been reported to play an important role in the pathogenesis of indomethacin-induced small intestinal injury. In this study, we investigated the role of mast cells in indomethacin-induced small intestinal injury using mast cell deficiency (Ws/Ws) rat.

Methods: Ws/Ws rats and control (W+/W+) rats were given indomethacin (15 mg/kg) subcutaneously, and the intestinal mucosal damage was estimated after 24 h.

Results: The area (mm2) of macroscopic visible lesions, the concentrations of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation, myeloperoxidase (MPO) activity as an index of neutrophil accumulation, and the content of cytokine-induced neutrophil chemoattractant-1 (CINC-1) were significantly increased in indomethacin-treated groups compared with the sham groups. The development of intestinal lesions in response to indomethacin was prevented in Ws/Ws rats compared with W+/W+ rats, together with significant suppression of the increased levels of TBARS, MPO activities, and CINC-1 levels.

Conclusions: These results indicate that mast cells are involved in the pathogenesis of the intestinal mucosal damage induced by indomethacin.

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