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Gastroenterology Research and Practice
Volume 2012 (2012), Article ID 362536, 8 pages
http://dx.doi.org/10.1155/2012/362536
Research Article

Does Cisapride, as a 5HT4 Receptor Agonist, Aggravate the Severity of TNBS-Induced Colitis in Rat?

1Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan 8146-73461, Iran
2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan 8146-73461, Iran
3Department of Clinical Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan 8146-73461, Iran
4Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz 8146-73461, Iran
5Islamic Azad University, Qazvin Branch, Qazvin 8146-73461, Iran

Received 31 May 2012; Revised 9 June 2012; Accepted 9 June 2012

Academic Editor: A. Andoh

Copyright © 2012 Azadeh Motavallian et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

There is a pressing need for research that will lead to the reveal of targets designed to analyse the possible pathways for the treatment of IBD. Because of the probable involvement of serotonin in inflammatory conditions of intestine and the important role of 5HT4 receptors in GI function, the investigation of the role of 5HT4 receptors in the pathogenesis of IBD will be interesting. The aim of this study was to investigate the effects of cisapride, a 5HT4 receptor agonist, in trinitrobenzenesulfonic-acid-(TNBS) induced rat colitis. Two hours subsequent to induction of colitis using TNBS in rats, cisapride (2 mg/kg, intraperitoneally (i.p); 4 mg/kg, orally (p.o)) and dexamethasone (1 mg/kg, i.p; 2 mg/kg, p.o) were administrated for 6 days. Animals were thereafter euthanized; macroscopic, histological, and biochemical assessments and ELISA test were carried out on distal colon samples. Our data showed that dexamethasone treatment (i.p, p.o) significantly decreased macroscopic and microscopic damage and also biochemical markers, but there were no significant differences in aforementioned parameters between cisapride (i.p or p.o) and TNBS-treated rats. It can be deduced that because the severity of colitis produced by TNBS is massive (through various pathways), cisapride could not bring about more colitis damages through 5HT4 receptors. Based on the present study further researches are required for investigating the exact roles of 5HT4 receptors in the pathogenesis of ulcerative colitis.