Effect of Clostridium Butyricum to promote the intestinal barrier of DSS colitis by regulating endogenous hydrogen sulfide enzyme

Background: Although Clostridium Butyricum ameliorates active ulcerative colitis (UC), the precise mechanism remains largely unclear. To investigate the mechanism of Clostridium Butyricum in protecting intestinal barrier of DSS colitis by regulating endogenous hydrogen sulfide enzyme. Methods: Forty C57BL/6J male mice were randomly divided into control group, DSS colitis group, low-dose (10 7 CFU/ml) Clostridium Butyricum group and high-dose (10 8 CFU/ml) Clostridium Butyricum group. We use qRT-PCR and Western blot to assess the expression of CSE and CBS as endogenous hydrogen sulfide enzyme in colonic tissue of each group. However, the expression of ZO-1,Occludin, E-cadherin, Lypd8, MIF and DAI score, colon length, histological damage were separately used to evaluate the epithelial tighten junction, mucous barrier and epithelial inflammation in intestine. Result: Both high-dose and low-dose live Clostridium Butyricum could significantly diminish the expression of CSE, CBS of colonic tissue in DSS colitis ( P<0.05 ). The live Clostridium Butyricum dose-dependently inhibited the colonic length shorten, DAI scores and histological damage of DSS colitis with down-regulating the expression of MIF and increasing the expression of ZO-1, Occludin, E-cadherin and Lypd8 in DSS colitis ( P<0.05 ). Conclusions: The live Clostridium Butyricum ameliorates DSS colitis by suppressing the expression of CSE and CBS with the mechanism related to regulate the epithelial mucous barrier protein, protect the epithelial tighten junction and inhibit the inflammatory factor with the possible down-regulating the expression of hydrogen sulfide (H 2 S).