【摘 要】
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Background and Aims: Disequilibrium of the mucous barrier is central to the pathogenesis and further exacerbation of inflammatory bowel disease.Our aim was to investigate whether butyrate can ameliora
【机 构】
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Wuxi People's Hospital
【出 处】
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2017中国医师协会消化医师分会年会
论文部分内容阅读
Background and Aims: Disequilibrium of the mucous barrier is central to the pathogenesis and further exacerbation of inflammatory bowel disease.Our aim was to investigate whether butyrate can ameliorate spontaneous colitis,modulate the mucus barrier and decrease bacteria penetration in Il10-/-mice,a classic animal model of inflammatory bowel disease.Methods: Male wild type mice and Il10-/-mice aged 12-16 weeks were assigned to the WTgroup,the IL-10-KO group and the butyrate group (n=6~8 in each group).Mice in the butyrate group received sodium butyrate sodium (100mM) in the drinking water,and mice in the WT group and the IL-10-KO group received normal drinking water as vehicle.After 4 weeks,mice were sacrificed for analysis.Severity of colitis,adherent bacteria load,integrity of mucus barrier,mucus bacterial penetration,mucus thickness and number of goblet cells were measured.Furthermore,the expression of autography associated protein in goblet cells was also assessed.Results: The 4-week butyrate treatment ameliorated spontaneous colitis,down-regulated bacteria translocation and adherent bacteria,increased the thickness of inner mucus layer,and reduced mucus bacterial penetration scores in Il10-/-mice.Moreover,the suppressed expression of autography associated protein in goblet cells in Il10-/-mice was restored after butyrate treatment.Conclusions: Butyrate treatment ameliorates colitis,modulates the mucus barrier and decreases mucus bacteria penetration in Il10-/-mice,which is associated with restored autophagy function in goblet cells.Our study may support the therapeutic approach to inflammatory bowel disease.
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