ABSTRACT
Objective To evaluate the effects of probiotics in experimental colitis of rats.Methods Models of experimental colitis were established.Several groups of rats were set up as probiotics group,negative group and positive group.Histologic scoring was used to estimate effects of drugs;the expression of CD~+_4 andCD~+_8 on T cell surface in peripheral blood,spleen mononuclear cells and intraepithelial lymphocytes of colon were detected by flow cytometry.Results Histopathology shows that probiotics of larger dosage was curative for experimental colitis in rats.Proportion of CD~+_4 and CD~+_8 T cells increased in colon of colitis,which was decreased by treatment of larger dose of probiotics.CD~+_4/CD~+_8 ratio and T cell subsets in systemic immune system were not influenced by probiotics.Conclusion Probiotics of large dosage are effective in the treatment of experimental colitis of rats incuced by TNBS,possibly associated with immune regulation and tends to be localized in mucosal immune system in colon.
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Objective To evaluate the effects of probiotics on experimental colitis of rats and to explore systemic and local changes of T regulatory cells(Tr) after the treatment. Methods The models of experimental colitis were established by enema with 2,4,6-trinitrobenzenesulphonic acid (TNBS). Live probiotics of combined bifidobacterium,lactobacillus and enterococcus (Bifico) were used. Four groups of rats were set up as negative group, TNBS alone group, probiotics group (high dosage and low dosage, with dose of 150 and 300 mg?kg-1?d-1, respectively), and combination group (probiotics plus prednisolone or sulfasalazine). Histologic scoring was used to evaluate the effect of medications; the proportions of CD4+CD25+ and CD8+CD28- Tr in peripheral blood, spleen mononuclear cells and intraepithelial lymphocytes of colon were detected by flow cytometry. Results Histopathology showed that high dosage of probiotics was effective in TNBS-induced colitis rats (2. 2?0.8 vs 3.5?0.7,P
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Objective Zinc sulfate has anti inflammatory action in many animal models, however, the effects of zinc in colitis remained uncertain. The present study was to evaluate the role of zinc sulfate in experimental colitis and probe into its underlying mechanisms. Methods Colitis was induced by administrating 2,4,6 trinitrobenzenesulphonic acid (TNB) rectally in Spragur Dawley female rats. Beginning at the first day of TNB colitis, the rats were treated with zinc sulfate enema once daily for 6 days. The rats were sacrificed at days 8. The effects of zinc sulfate were evaluated by examining mucosal lesion area, mucosal myeloperoxidase (MPO) and superoxide dismutase (SOD) activities, mucosal prostaglandin E 2(PGE 2) and leukotriene B 4(LTB 4) levels. Results TNB induced severe colitis as evidenced by increased mucosal lesion area, mucosal MPO activity and PGE 2 and LTB 4 levels. Six days after the application of the zinc sulfate enema, the mucosal lesion area, MPO activity, PGE 2 and LTB 4 levels were all decreased significantly, except mucosal SOD activity that was remained unchanged after zinc treatments. Conclusions The data suggest that zinc sulfate enemas have an anti inflammatory action on experimental colitis through the mechanism other than increasing SOD activity.
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Objective:To investigate costimulatory molecules and adhension molecules in the pathogenesis of experimental colitis in rats.Methods:Models of experimental colitis were established by enema with trinitrobenzenesulphonic acid. Prednisolone or salicylazosulfapyridine was given as treatment.Nomal rat and untreated colitis rat groups were set up as controls.Histological scoring was performed.Expression of CD11b,CD28 and CTLA-4 were detected by flow cytometry in peripheral blood,spleen and intraepithelial mononuclear cells of colon.Results:Expressions of CD11b,CD28 and CTLA-4 were high in experimental colitis. CD11b and CD28 decreseased after treatment of prednisolone or salicylazosulfapyridine,while CTLA-4 increased further,which were significant statistically.Conclusion:Adhesion molecules may have a role in the pathogenesis of experimental colitis.The dysregulation of CD28 and CTLA-4 may be one of the mechanisms in IBD.The mechanisms of prednisolone and salicylazosulfapyridine may be associated with costimulatory molecules and adhension molecules.