ABSTRACT
Inflammatory bowel disease(IBD)is a kind of chronic and non-specific inflammatory disease comprising Crohn’s disease(CD)and ulcerative colitis(UC),the etiology has not yet been clarified. Endothelin-1(ET-1)is an active polypeptide composed of 21 amino acid residues,which can constrict blood vessels by activating voltage-dependent Ca2 + channels in vascular smooth muscle cells. Studies have shown that ET-1 plays an important role in the pathogenesis of IBD. This article reviewed the progress in study on ET-1 in the pathogenesis of IBD.
ABSTRACT
AIM:To investigate the effect of mesalazine treatment on regulation of Th1, Th17 and Treg cells in mice with dextran sulfate sodium ( DSS)-induced ulcerative colitis ( UC) .METHODS:The expression of IL-17, IFN-gam-ma and Foxp3 in the peripheral blood mononuclear cells ( PBMC) and intestinal mucosa lamina propria mononuclear cells ( LPMC) of DSS-induced UC mice was detected by flow cytometry analysis.The effect of mesalazine treatment on regulaiton of Th1, Th17 and Treg cells in the mice with DSS-induced ulcerative colitis was examined.RESULTS:The expression of IL-17, IFN-γand Foxp3 on CD4 +T cells were significantly higher in the PBMC of DSS-induced mice than those in control group.CD4+IFN-γ+T cells and CD4 +Foxp3 +T cells were higher in LPMC than those in control group, except CD4+IL-17 +T cells.Moreover, the Th1, Th17 and Treg cells were higher in DSS group than those in control group in LPMC.How-ever, only Tregs was higher in PBMC.Pre-treatment with mesalazine significantly decreased the number of Th17, Th1 and Treg cells of UC model mice both in PBMC and LPMC.CONCLUSION: The Th1, Th17 and Tregs cells in DSS-induced mice were significantly higher than those in control mice, suggesting that CD4 +T cell subsets play an important role in the pathogenesis of UC.Mesalazine may play a role in the treatment of UC by regulating the Th1, Th17 and Tregs cells.