1. Introduction
Ulcerative colitis (UC) and Crohn’s disease (CD) are the main two types of inflammatory bowel disease (IBD) [1]. A disturbed intestinal immune response to the luminal microbiota is a well-recognized theory for IBD pathogenesis [2].
The ingested food stimulates the release of Glucagon-like peptides (GLPs); GLP-1 and GLP-2 from the intestinal enteroendocrine cells; L cells. GLP-1 is mainly concerned with lowering blood glucose by: stimulating the release of insulin from islet β cells and delaying gastric emptying [3-5]. In the same context, GLP-2 has the ability to restore intestinal homeostasis through its trophic effects on the intestinal epithelium, so it is currently used for treatment of short bowel syndrome (SBS) [6,7].
Both GLPs are degraded by dipeptidyl peptidase-IV (DPP-IV) enzymes [5], therefore DPP-IV inhibitors as well as GLP-1 are used to treat patients with type 2 diabetes mellitus (T2DM), as a monotherapy or in combination with other anti-diabetic drugs [8,9]. However, many experimental animal studies have proved that GLPs-based therapy has pivotal anti-inflammatory actions on various organs [10,11].
The aim of this work was to investigate the possible beneficial actions of the GLP-1; liraglutide and the DPP-IV inhibitor; sitagliptin, in treatment of UC induced experimentally in mice, in comparison with sulfasalazine, and to determine their tolerability and the possible underlying mechanism of action.