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World J Gastroenterol. 2014 Nov 28;20(44):16690-7. doi: 10.3748/wjg.v20.i44.16690.

Alleviated mucosal and neuronal damage in a rat model of Crohn's disease.

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Petra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.



To establish a rat model suitable to investigate the repetitive relapsing inflammations (RRI) characteristic to Crohn's disease.


Colitis was induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). RRI were mimicked by repeating administrations of TNBS. Tissue samples were taken from control, once, twice and three times treated rats from the inflamed and adjacent non-inflamed colonic segments at different timepoints during the acute intestinal inflammation. The means of the ulcerated area were measured to evaluate the macroscopic mucosal damage. The density of myenteric neurons was determined on whole mounts by HuC/HuD immunohistochemistry. Heme oxygenase-1 (HO-1) expression was evaluated by molecular biological techniques.


TNBS-treated rats displayed severe colitis, but the mortality was negligible, and an increase of body weight was characteristic throughout the experimental period. The widespread loss of myenteric neurons, and marked but transient HO-1 up-regulation were demonstrated after the first TNBS administration. After repeated doses the length of the recovery time and extent of the ulcerous colonic segments were markedly decreased, and the neuronal loss was on a smaller scale and was limited to the inflamed area. HO-1 mRNA level was notably greater than after a single dose and overexpression was sustained throughout the timepoints examined. Nevertheless, the HO-1 protein up-regulation after the second TNBS treatment proved to be transient. Following the third treatment HO-1 protein expression could not be detected.


Experimentally provoked RRI may exert a protective preconditioning effect against the mucosal and neuronal damage. The persistent up-regulation of HO-1 mRNA expression may correlate with this.


Crohn’s disease; Experimental rat model; Heme oxygenase-1; Myenteric neurons; Repetitive relapsing inflammation

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