【摘要】 目的探讨低聚果糖对溃疡性结肠炎(UC)模型小鼠肠黏膜屏障的调节作用及可能机制。方法小鼠随机分成3组:正常对照(NC)组、模型(MD)组和低聚果糖(FOS)组,采用葡聚糖硫酸钠制作UC小鼠模型。造模7d同时给予干预治疗,停用造模药物并后续治疗7d。采用细菌定量测定法检测肠道菌群,放射免疫法检测肠黏膜sIgA,ELISA法检测小鼠肠黏膜IL-10、TNF-α和IL-6水平。结果模型组小鼠存在肠道菌群失调(t=2.088,2.036,2.203,2.109,P<0.05),其TNF-α、IL-6水平高于正常对照组(t=1.734,1.801,P<0.05),肠黏膜sIgA、IL-10低于正常对照组(t=1.820,1.806,P<0.05);低聚果糖组肠道菌群失调状况较模型组有所改善,其TNF-α、IL-6水平低于正常对照组(t=1.980,1.816,1.936,1.920,1.969,1.893,P<0.05),肠黏膜sIgA、IL-10高于正常对照组(t=1.801,1.796,P<0.05)。结论低聚果糖可改善溃疡性结肠炎模型小鼠肠道菌群屏障功能,可以提高肠黏膜sIgA和抗炎细胞因子IL-10的水平并降低致炎细胞因子TNF-α和IL-6的水平,通过调节肠道过度的免疫反应,使免疫屏障功能得到一定恢复。更多还原

【Abstract】 Objective To explore the regulatory effect and the possible mechanism of fructo oligosaccharides(FOS)to the intestinal barrier of mouse models with ulcerative colitis.Methods The mice were randomly divided into the Control group,Model group or FOS group.Ulcerative colitis was induced by oral administration of synthetic dextran sulfate sodium for 7days;intervention treatment with FOS was given to FOS group simultaneously during the modeling and lasted for 7more days after modeling.The quantity of intestinal flora was measured by quantitative detection;the level of sIgA in intestinal mucous membrane was detected with radioimmunity;the levels of IL-10,TNF-αand IL-6were detected by using ELISA method.Results(1)Dysbacteria was observed in model group;the levels of sIgA and IL-10 in intestinal mucous membrane were lower(P<0.05),while the levels of TNF-αand IL-6were higher(P<0.05)in model group than in the control group.(2)The symptoms of dysbacteria had been improved in FOS group;the levels of sIgA and IL-10 in intestinal mucous membrane were higher(P<0.05),while the levels of TNF-αand IL-6were lower(P<0.05)in FOS group than in the model group.Conclusion FOS can improve the function of intestinal barrier,up-regulate the levels of sIgA and IL-10 while down-regulate the levels of TNF-αand IL-6,and enhance the immune barrier function in a certain extent.更多还原