Objective: To observe the effects of Saccharomyces boulardii (Sb) on theTNBS-induced BALB/C mice colitis, and to explore its possible mechanism.Methods: Thirty BALB/C male mice were randomly divided into two groups with aratio of1:2, group A (control group, n=10) and group B (studied group, n=20). Themice in group A were treated with saline enema, and in group B with enema ofethanol-TNBS solution. After successfully modelled, the mice in group B weresubdivided randomly into group C (treated with gavage of normal saline) and groupD (gavage of Sb solution) for7days. The mice general condition, weight, survivalrate were observed and recorded. The animals were killed, and the macro-and micro-,inflammation scores were recorded. The expression of TLR2, medullary factor88(MyD88), and TNF–α concentration in intestinal tissue were measured by immuno-histochemistry, and ELISA respectively.Results: The survival rat of groups C and D (both50%) showed no significantdifference. The mice of group C (2.00±0.89) and group D (1.83±0.75) showedhigher generally intestinal tissue inflammation scores than in group A (0.00±0.00),(group C vs group A: χ2=144.63, P <0.005; group D vs group A: χ2=128.03, P<0.005), the difference between group C and D was no statistically significant (P>0.05). Meanwhile, microscopic inflammation scores in the group C (3.50±0.55) andgroup D (2.67±0.52) also showed higher than in the group A (0.30±0.15)(group Cvs group A: χ2=181.53, P <0.0005; group D vs group A: χ2=87.00P <0.005), but itwas lower in group D (χ2=13.75, P <0.05). The levels of TNF-α (1367.93±171.59),TLR2(0.007±0.002) and MyD88(0.09±0.02) in intestinal tissue of Group D werehigher than group A (P <0.05), but TNF-α, TLR2, MyD88levels in Group D werelower than in group C (TNF-α1079.71±181.51; TLR20.019±0.009; MyD880.02±0.02)(P <0.05). Conclusions: The gavage of Sb does not improve the survival rates in BALB/C micewith TNBS-induced colitis. However it could inhibit the colonic inflammation, whichmay be contributed to its inhibitory effect on the expression of TLR2, MyD88, andTNF-α. These suggest that Sb may play an inhibitory role in the TNBS-induced colitisby the TLR2-MyD88-dependent pathway. |