Background: Low-grade inflammation may play a role in the pathogenesis of IBS. Although corticosteroids are potent inhibitors of inflammatory processes, only one study with corticosteroids in patients with post-infectious IBS exists and suggests that prednisolone is not an effective treatment for IBS symptoms.
Aim: The aim of this study was to evaluate if dexamethasone treatment prevents PAR-2 activation- induced visceral hyperalgesia and increased permeability in rats, and to determine if the effects involve colonic mast cells.
Methods: Abdominal contractions provoked by rectal distension were recorded in rats equipped with intramuscular electrodes. Changes in visceral hypersensitivity provoked by intracolonic administration of PAR-2 activating peptide (SLIGRL), changes in colonic mucosal RMCP-II content, mast cell count and PAR-2 expression were measured after 4 day treatment with dexamethasone (1mg/day/rat ip) or its vehicle (water). Effect of mast cell stabilizer (doxantrazole, 1mg/kg ip, 2 hours before and 6 hours after intracolonic infusion of SLIGRL) on SLIGRL induced visceral hyperalgesia was also assessed. Effects of SLIGRL and a mast cell degranulator (C48/80) on permeability of colonic strips from vehicle or dexamethasone-treated rats were investigated in Ussing chambers.
Results: Four days of dexamethasone as well as doxantrazole, diminished the SLIGRL-induced hyperalgesia for all volumes of distension. This effect of dexamethasone was accompanied by a reduced responsive of colonic permeability to C48/80and decreased RMCP-II content and mast cell number. Dexamethasone treatment did not influence colonic mucosal PAR-2 expression and permeability responsiveness to SLIGRL.
Conclusions: Dexamethasone treatment improves PAR- 2 agonist-induced visceral hypersensitivity but does not prevent PAR-2 agonist-induced increase in colonic permeability in rats. This effect is coupled with a reduction of colonic mast cell number and RMCP-II contents.
- PAR-2 activation
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