首页|基于肠道炎症反应研究降糖3号方抗糖尿病的作用机制

基于肠道炎症反应研究降糖3号方抗糖尿病的作用机制

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  • 国家科技期刊平台
  • NETL
  • NSTL
  • 万方数据
目的:观察降糖3号方对2型糖尿病小鼠肠道炎症相关指标的影响,揭示其抗糖尿病的作用机制.方法:选取4周龄C57BL/6N雄性小鼠,高脂饲料联合小剂量链脲佐菌素(STZ)注射构建2型糖尿病小鼠模型,采用随机数字表法将成模小鼠分成模型组、二甲双胍组、降糖3号方组,每组8只.选取8只标准饲料喂养的小鼠作为正常组.药物干预8周结束后,应用细胞因子抗体芯片技术检测小鼠结肠组织中多种炎症介质水平,并进行差异表达蛋白筛选、基因本体(GO)蛋白功能、京都基因和基因组百科全书(KEGG)通路分析.蛋白质印迹法检测各组小鼠结肠组织中核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体激活与肠道黏膜屏障相关的因子G蛋白偶联受体43(GPR43)、凋亡相关斑点样蛋白(ASC)、胱天蛋白酶(Caspase-1)以及闭锁小带蛋白-1(ZO-1)、闭合蛋白(Occludin)的蛋白表达水平.结果:各组间肠道炎症介质差异明显,与模型组比较,降糖3号方组IL-1β、IL-6等炎症介质表达下降,降糖3号方可上调结肠组织中ZO-1、Oc-cludin、GPR43 蛋白表达水平,降低ASC、Caspase-1蛋白表达水平(P＜0.05).结论:2型糖尿病小鼠结肠炎症反应明显,降糖3号方能够有效抑制2型糖尿病小鼠肠道炎症,其作用可能与调控NLRP3炎症小体,进而影响下游炎症介质有关.
Anti-diabetic Mechanism of Jiang Tang San Hao Formula Based on Intestinal Inflammation
Objective:To observe the effect of Jiang Tang San Hao Formula(JTSHF)on intestinal inflammation in the mouse mod-el of type 2 diabetic mellitus(T2DM)and reveal the anti-diabetic mechanism of JTSHF.Methods:Four-week-old C57BL/6N male mice were selected for the modeling of T2DM by a high-fat diet combined with injection of low-dose streptozotocin(STZ).The mod-eled mice were then randomized into a model group,a metformin group,and a JTSHF group,with 8 mice in each group.Eight mice were fed with a standard diet and served as the normal group.All the mice were administrated with corresponding drugs for 8 weeks.The cytokine antibody array kit was used to determine the levels of multiple inflammatory mediators in the colon tissue of mice.The differentially expressed proteins were screened,which was followed by Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment.Western blotting was employed to determine the activation of nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain-containing protein 3(NLRP3)inflammasome and the expression levels zonula occludens-1(ZO-1),occludin,G protein-coupled receptor 43(GPR43),apoptosis-associated speck-like protein containing a CARD(ASC),and caspase-1 in the colon tissue of mice.Results:The levels of inflammatory mediators in the colon tissue differed significantly between groups.Compared with the model group,the JTSHF group showed lowered levels of interleukin-1β(IL-1β)and IL-6,up-regulated expression of ZO-1,occludin,and GPR43,and down-regulated expression of ASC and caspase-1(P＜0.05).Conclusion:Obvious inflammation was observed in the colon tissue of T2DM mice,which was reduced by JTSHF.JTSHF may regulate the NLRP3 inflammasome and its downstream inflammatory mediators to exert the therapeutic effect.

Type 2 diabetes mellitusJiang Tang San Hao FormulaInflammatory mediatorsNucleotide-binding oligomerization do-main leucine-rich repeat and pyrin domain-containing protein 3(NLPR3)inflammasomeAntibody arrayColon tissueMechanism

赵祎、徐冰蕊、叶紫梦玮、莫芳芳、穆倩倩、田甜、杨晓达、高思华、赵丹丹

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北京中医药大学中医学院,北京,100029

北京中医药大学东直门医院,北京,100007

北京大学医学部,北京,100191

糖尿病 降糖3号方 炎症介质 核苷酸结合寡聚化结构域样受体蛋白3炎症小体 抗体芯片 结肠组织 作用机制

国家自然科学基金项目国家中医药领军人才支撑计划-岐黄学者项目北京中医药大学基本科研业务费揭榜挂帅项目北京市中医药管理局科技发展基金项目

8217432910400633210052023-JYB-JBZD-010JJ2018-72&JJ2018-72

2024

10.3969/j.issn.1673-7202.2024.08.005

世界中医药
世界中医药学会联合会

世界中医药

CSTPCDCHSSCD北大核心
影响因子：1.266
ISSN：1673-7202
年,卷(期)：2024.19(8)