OBJECTIVE.
Mesalazine, from which
5-aminosalicylic acid is released, is a therapeutic
drug for
inflammatory bowel disease. There has been no study concerning the effect of orally administered
mesalazine on
dextran sodium sulfate (DSS)-induced
colitis in the rat model of
ulcerative colitis. MATERIAL AND METHODS.
Colitis was evaluated by means of the length of the colon, white blood cell count (WBC), tissue
myeloperoxidase (MPO) activity, and histological
inflammation scores. Colonic mucosal permeation was evaluated using
Evans blue. The localization of a
tight junction protein,
occludin, was evaluated immunohistochemically and examined using confocal
laser scanning microscopy. RESULTS.
Mesalazine significantly improved changes in the length of the colon, tissue MPO activity, WBC, and the histological
inflammation score as compared with DSS-induced
colitis. Furthermore, the
drug completely inhibited the increased permeation in DSS-induced
colitis in rats. The immunofluorescence signals of
occludin were disrupted and irregularly distributed in DSS-induced
colitis, while the signals appeared as a typical reticular pattern but with reduced intensity by the administration of
mesalazine, without any reduction in the
protein content. In addition, the
oral administration of
mesalazine significantly improved mucosal permeation, thereby protecting the intestinal mucosa against injury in DSS-induced
colitis in rats. CONCLUSIONS. These findings suggest that the recovery of mucosal impairment due to treatment with
mesalazine may be associated with the protection of the
tight junction protein occludin in DSS-induced
colitis.