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.