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作 者:沈媛媛[1] 程凯[2] 张冉冉[1] 刘成霞[1] SHEN Yuanyuan;CHENG Kai;ZHANG Ranran;LIU Chengxia(Department of Gastroenterology,Binzhou Medical University Hospital,Binzhou 256603,Shandong,P.R.China;Department of Thyroid Surgery,Binzhou Medical University Hospital,Binzhou 256603,Shandong,P.R.China)
机构地区:[1]滨州医学院附属医院消化内科,山东滨州256603 [2]滨州医学院附属医院甲状腺外科,山东滨州256603
出 处:《滨州医学院学报》2022年第4期257-260,272,共5页Journal of Binzhou Medical University
基 金:山东省医药卫生科技发展计划(2018WS544)。
摘 要:目的探讨酪酸梭菌调控肠道菌群对溃疡性结肠炎的作用机制。方法将30只C57BL/6J小鼠随机分为正常对照组、葡聚糖硫酸钠(DSS)结肠炎组和酪酸梭菌组,每组10只。给予小鼠饮用3.5%DSS溶液7 d以建立DSS结肠炎模型,同时给予108CFU酪酸梭菌活菌灌胃处理酪酸梭菌组小鼠。采用16S微生物群落多样性组成谱分析三组小鼠的粪肠道菌群物种组成差异,采用DAI评分、结肠长度及HE染色评估结肠炎症程度,采用ELISA测定血清TNF-α,采用免疫组化法观察闭锁小带蛋白1(ZO-1)及Occludin。结果DSS结肠炎组小鼠的粪便脱硫弧菌属丰度升高,酪酸梭菌处理结肠炎小鼠后,降低了粪便脱硫弧菌属丰度,显著降低DAI评分、抑制结肠长度短缩及镜下粘膜炎症程度,下调血清TNF-α水平,上调表达ZO-1及Occludin水平,P<0.05。结论酪酸梭菌通过抑制粪便脱硫弧菌属,减少促炎因子TNF-α、增加紧密连接蛋白保护肠黏膜屏障,达到抑制DSS结肠炎的生物学作用。Objective To investigate the effect of Clostridium butyricumon ulcerative colitis by regulating the intestinal microbiota.Methods Thirty C57 BL/6 J mice were randomly divided into the normal control group,the DSS colitis group and the Clostridium butyricum treated group,with 10 mice in each group.The mice were fed 3.5%DSS solution for 7 days to induce DSS colitis,and treated with 108 CFU live Clostridium butyricum by gastric intubation in the Clostridium butyricum treated group.All the mice were assessed fecal intestinal microbiota diversity by 16 Smicrobial community diversity composition;intestinal inflammation was evaluated with DAI scores,colon length and HE staining;the expression of TNF-αin serum was determined by ELISA and the expression of tissue tight junction protein as ZO-1 and Occludin were observed with immunohistochemistry.Results The fecal Desulfovibrio levels of the DSS colitis group increased;the administration of Clostridium butyricum for DSS colitis decreased the level of fecal Desulfovibrioin stool,significantly decreased DAI scores,inhibited the colon length shortening and mucosal inflammation under microscope,down-regulated the levels of serum TNF-α,and up-regulated the levels of ZO-1 and Occludin,(P<0.05).Conclusion Clostridium butyricum can effectively ameliorate DSS colitis and protect the intestinal mucosal barrier by regulating the level of fecal Desulfovibrioas,decreasing TNF-α,and increasing the tight junction protein.
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