Advances in Clinical and Experimental Medicine
2018, vol. 27, nr 5, May, p. 599–607
Publication type: original article
Comparison of two models of inflammatory bowel disease in rats
1 Department of Medical Biochemistry, “Iuliu Haţieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania
2 Department of Parasitology and Parasitic Diseases, University of Agricultural Sciences and Veterinary Medicine, Cluj-Napoca, Romania
3 Department of Anatomic Pathology, Necropsy and Forensic Medicine, University of Agricultural Sciences and Veterinary Medicine, Cluj-Napoca, Romania
4 Department of Pharmaceutical Biochemistry and Clinical Laboratory, “Iuliu Haţieganu“ University of Medicine and Pharmacy, Cluj-Napoca, Romania
5 Research Center for Functional Genomics, Biomedicine and Translational Medicine, “Iuliu Haţieganu“ University of Medicine and Pharmacy, Cluj-Napoca, Romania
6 Medfuture Research Center for Advanced Medicine, Cluj-Napoca, Romania
7 Department of Functional Genomics and Experimental Pathology, The Oncology Institute
8 2nd Medical Department, “Iuliu Haţieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania
Background. There is a need for experimental animal models for inflammatory bowel diseases (IBD), but no proposed model has been unanimously accepted.
Objectives. The aim of this study was to develop 2 affordable models of IBD in rats and to compare them.
Material and Methods. We produced IBD in rats using either dextran sodium sulfate (DSS) or 2, 4, 6-trinitrobenzene sulfonic acid (TNBS). The requirements for experimental models were: a predictable clinical course, histopathology and inflammation similar to human ulcerative colitis (UC) and Crohn’s disease (CD). The effect of acute administration of DSS and TNBS on oxidative stress (as measured by the assessment of glutathione peroxidase – GPx) was verified. The activity of whole blood GPx was measured using a commercially available Randox kit (Crumlin, UK).
Results. The administration of DSS increased GPx activity compared to the control and TNBS-treated groups, but not to a statistically significant degree. Histological examination of the colonic mucosa following the administration of DSS showed multifocal erosions with minimal to mild inflammatory infiltrate, mainly by polymorphonuclear cells (PMN), lymphocytes and plasma cells. For TNBS-induced colitis, the histological changes manifested as multifocal areas of ulcerative colitis with mild to severe inflammatory infiltrate. Whole blood GPx values displayed a direct dependence on the chemical agent used. Our results show a correlation between histopathology, proinflammatory state and oxidative stress.
Conclusion. The experimental DSSor TNBS-induced bowel inflammation used in this study corresponds to human IBD and is reproducible with characteristics indicative of acute inflammation in the case of the protocols mentioned.
animal model, colitis, dextran sodium sulfate, 2, 4, 6-trinitrobenzene sulfonic acid, inflammatory bowel disease
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