微生物多糖调控克罗恩病肠道炎症免疫反应的机制研究  

Mechanism of Microbial Polysaccharides Regulating Intestinal Inflammatory Immune Response in Crohn's Disease

作　　者：刘威 黄文峰[1] 周云[1] 孟凡[1] 何良梅 LIU Wei;HUANG Wenfeng;ZHOU Yun;MENG Fan;HE Liangmei(The First Affiliated Hospital of Gannan Medical College,Ganzhou Jiangxi 341000,China)

机构地区：[1]赣南医学院第一附属医院,江西赣州341000

出　　处：《药品评价》2022年第18期1108-1111,共4页Drug Evaluation

基　　金：江西省教育厅科学技术研究项目(GJJ211508)。

摘　　要：目的:研究微生物多糖调控克罗恩病肠道炎症免疫反应的机制。方法:选取60只健康雄性BABL/c小鼠,将小鼠随机分为三组,分别为对照组、模型组及实验组,每组20只。实验组和模型组小鼠建立克罗恩病模型,实验组小鼠给予灌胃已制备好的微生物多糖溶液0.25 mL/次,模型组和对照组小鼠灌胃等量的无菌水,2次/d,连续21 d。检测各组小鼠疾病活动度评分、组织病理学评分及相关通路蛋白。结果:与对照组相比,模型组和实验组小鼠DAI评分明显升高;与模型组相比,实验组小鼠DAI评分明显降低(P<0.05)。与对照组相比,模型组及实验组小鼠组织病理学评分明显升高;与模型组相比,实验组小鼠组织病理学评分显著降低(P<0.05)。与对照组相比,模型组和实验组血清促炎因子TNF-α、IL-1β、IL-6表达水平升高,IL-10表达水平降低;与模型组相比,实验组血清促炎因子TNF-α、IL-1β、IL-6表达水平降低,IL-10表达水平升高(P<0.05)。与对照组相比,模型组和实验组小鼠结肠组织炎性因子Toll-样受体4(TLR4)、髓样分化蛋白抗原88(MyD88)、核因子кB p65(NF-κBp65)蛋白表达水平均明显升高;与模型组相比,实验组小鼠结肠炎性因子TLR4、MyD88、NF-κBp65蛋白表达均明显下降(P<0.05)。结论:微生物多糖通过调控TLR4/MyD88/NF-κB信号通路调控克罗恩病肠道炎症免疫反应的机制。Objective:To study the mechanism of microbial polysaccharides regulating intestinal inflammatory immune response in Crohn's disease.Methods:Sixty healthy male BABL/c mice were randomly divided into three groups:control group,model group and experimental group,with 20 mice in each group.Crohn's disease model was established in experimental group and model group mice.The mice in experimental group were given 0.25 mL/time of prepared microbial polysaccharide solution by gavage,and the mice in model group and control group were given the same amount of sterile water by gavage,twice a day for 21 days.The disease activity score,histopathological score and related pathway proteins of mice in each group were detected.Results:Compared with control group,the DAI scores of mice in model group and experimental group were significantly higher;compared with model group,the DAI score of experimental group mice was significantly lower(P<0.05).Compared with control group,the histopathological scores of model group and experimental group mice were significantly higher;compared with model group,the histopathological score of experimental group mice was significantly lower(P<0.05).Compared with control group,the serum pro-inflammatory factor TNF-α、IL-1β、IL-6 increased and the expression level of IL-10 decreased in model group;compared with model group,the serum pro-inflammatory factor TNF-α、IL-1β、IL-6 decreased and the expression level of IL-10 increased in experimental group(P<0.05).Compared with control group,the inflammatory factors TLR4,MyD88,NF-κBp65 protein was significantly increased;compared with model group,colitis factors TLR4,MyD88,NF-κBp65 protein decreased significantly(P<0.05).Conclusion:Microbial polysaccharides regulate the mechanism of intestinal inflammatory immune response in Crohn's disease by regulating TLR4/MyD88/NF-κB signaling pathway.

关 键 词：克罗恩病 微生物多糖 肠道免疫反应 Toll-样受体4 髓样分化蛋白抗原88 核因子кB p65 小鼠 近交BABL/c 

分 类 号：R574.62[医药卫生—消化系统]