Effects Of Sodium Butyrate On Colonic Mucosal Reparation In TNBS-Colitis Model Rats

Background and Aims:The colonic mucosal inflammation damage and repair is a key character of inflammatory bowel disease (IBD). Sodium butyrate, a primary product of dietary fiber fermentation, plays an important role in maintaining colonic epithelial integrity and cell differentiation. The aims were to investigate the effects of sodium butyrate on colonic mucosal anti-inflammatory damage and repair in colitis model rats, and preliminary to explore the possible mechanisms of sodium butyrate in the treatment of IBD.Methods:A total of 48 Sprague-Dawley rats were randomly divided into four groups:normal control group (A group), colitis model group(B group), sodium butyrate treated-group (C group) and mesalazin-treated group (principal ingredient is 5-aminosalicylic acid, D group).Colitis model was induced by trinitrobenzene sulfonic acid (TNBS). The rats were killed separately on the acute and remission stage of colitis. Histological score of colon was evaluated. The expression of transforming growth factor-β1 (TGF-β1) and vascular endothelial growth factor(VEGF) in colonic mucosa were measured by immunohistochemistry (IHC).The levels of interleukin-8 (IL-8) and interleukin-10 (IL-10) in plasma were measured by enzyme-linked immunosorbent assay (ELISA). Results:Compared with B group, the general conditions and histology of colon in C group were slightly improved,But the D group were obviously improved. The expression of TGF-β1 in colonic mucosa of B group was lower than those in C group and D group. The expression of VEGF in colonic mucosa has no statistical significance among three groups. In the acute stage, Compared with A group,the levels of interleukin-8 (IL-8) in C group was higher, but compared with B group, the levels of interleukin-8 (IL-8) in C group has no statistical significance.After the treatment of sodium butyrate, in the remission stage, the levels of interleukin-8 (IL-8) and interleukin-10 (IL-10) in C group were respectively lower and higher than those in B group (p<0.05).Conclusions:Sodium butyrate displays the effect on colonic mucosal repair in colitis model rats. The mechanisms may be due to up-regulating the expression of TGF-β1 in colonic mucosa and regulating the secretion of plasma inflammatory cytokine IL-8 and anti-inflammatory cytokine IL-10.