Additionally, the stimulatory action of exogenous apelin on colonic epithelial proliferation suggests that the increased apelin production during intestinal recovery stage may contribute to the repair of the intestinal epithelium in experimental rodent models of colitis and in IBD patients.
MSM treatment also significantly reduced colonic levels of MDA, MPO and IL-1β, while increased the levels of GSH and CAT compared with acetic acid-induced colitis group.
We therefore investigated how treatment with Lactobacillus reuteri influenced P-selectin expression, leukocyte and platelet endothelial cell interactions, and colitis severity in DSS-treated rats.
Amelioration of experimental colitis by the selective beta(3)-adrenoceptor agonist SR58611A suggests that beta(3)-adrenoceptors may represent a therapeutic target in gut inflammation.
Glutamine inhibits over-expression of pro-inflammatory genes and down-regulates the nuclear factor kappaB pathway in an experimental model of colitis in the rat.
In summary, the present findings suggest a functional role for CXCR2 in initiating neutrophil recruitment during the early phase of TNBS-induced acute colitis, and demonstrate that: early colonic neutrophil accumulation is CXCR2 dependent and the late phase colonic neutrophil accumulation is CXCR2 independent.
In this study, we compared the usefulness of urinary vanin-1 with other newly developed biomarkers [urinary monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (Kim-1) and N-acetyl-beta-D-glucosaminidase (NAG)] for the detection of renal complications in rats with experimental colitis.
The results showed a significantly decreased BMP7 expression in the acute phase, followed by a significantly increased BMP2 and decreased BMP6 expression during the chronic phase of colitis.
Further experiments showed that colitis facilitated a retrograde transport of TrkA protein toward and an anterograde transport of TrkA mRNA away from the DRG, which may contribute to the increased TrkA mRNA level in the distal colon during colitis.
In colitis both the TrkA and TrkB protein levels were increased in the L1 and S1 DRGs in a time-dependent manner; however, the level of TrkB mRNA but not TrkA mRNA was increased in these DRGs.
De novo expression of both NK(1) and NK(2) receptor mRNA was observed during the acute phase of TNB-colitis in mesenchymal cells around dilated submucosal vessels but their expression in smooth muscle cells of the muscularis mucosae and propria was moderately down-regulated.