葛思堂, 张小凤, 何逸凡, 吴华涛, 张紫凝, 李静, 耿志军, 宋雪, 左芦根. EGCG对三硝基苯磺酸诱导的结肠炎小鼠肠道炎症和肠屏障功能的保护性作用和机制[J]. 蚌埠医学院学报, 2022, 47(1): 12-17. DOI: 10.13898/j.cnki.issn.1000-2200.2022.01.003
    引用本文: 葛思堂, 张小凤, 何逸凡, 吴华涛, 张紫凝, 李静, 耿志军, 宋雪, 左芦根. EGCG对三硝基苯磺酸诱导的结肠炎小鼠肠道炎症和肠屏障功能的保护性作用和机制[J]. 蚌埠医学院学报, 2022, 47(1): 12-17. DOI: 10.13898/j.cnki.issn.1000-2200.2022.01.003
    GE Si-tang, ZHANG Xiao-feng, HE Yi-fan, WU Hua-tao, ZHANG Zi-ning, LI Jing, GENG Zhi-jun, SONG Xue, ZUO Lu-gen. Protective effect and mechanism of EGCG on intestinal inflammation and intestinal barrier function in mice induced by trinitrobenzenesulfonic acid[J]. Journal of Bengbu Medical College, 2022, 47(1): 12-17. DOI: 10.13898/j.cnki.issn.1000-2200.2022.01.003
    Citation: GE Si-tang, ZHANG Xiao-feng, HE Yi-fan, WU Hua-tao, ZHANG Zi-ning, LI Jing, GENG Zhi-jun, SONG Xue, ZUO Lu-gen. Protective effect and mechanism of EGCG on intestinal inflammation and intestinal barrier function in mice induced by trinitrobenzenesulfonic acid[J]. Journal of Bengbu Medical College, 2022, 47(1): 12-17. DOI: 10.13898/j.cnki.issn.1000-2200.2022.01.003

    EGCG对三硝基苯磺酸诱导的结肠炎小鼠肠道炎症和肠屏障功能的保护性作用和机制

    Protective effect and mechanism of EGCG on intestinal inflammation and intestinal barrier function in mice induced by trinitrobenzenesulfonic acid

    • 摘要:
      目的探讨表没食子儿茶素没食子酸酯(EGCG)对2,4,6-三硝基苯磺酸(TNBS)诱导的结肠炎小鼠的作用效果以及可能的作用机制。
      方法选取24只雄性C57BL/6J小鼠,随机分为模型组(Model组)、对照组(WT组)和EGCG干预组(EGCG组),其中Model组和EGCG组小鼠采用TNBS诱导结肠炎。造模成功后,EGCG组给予腹腔注射15 mg·kg-1·d-1 EGCG干预,WT组和Model组给予等量0.9%氯化钠溶液。干预4周后,采用HE染色、免疫荧光法、Western blotting和细菌培养等技术,分析各组小鼠肠道炎症、肠黏膜炎症介质水平、肠屏障结构和功能以及结肠黏膜JAK2/STAT3信号改变情况。
      结果EGCG组小鼠体质量增长高于Model组(P < 0.05),与WT组相比差异无统计学意义(P>0.05)。干预第3~4周,EGCG组小鼠肠炎DAI评分明显低于Model组(P < 0.01)。干预4周后,EGCG组小鼠肠道炎症评分、肠黏膜IL-6和TNF-α水平均低于Model组(P < 0.05),但高于WT组(P < 0.05);同时肠上皮紧密连接蛋白Occludin和ZO-1水平均高于Model组(P < 0.05),与WT组相比差异无统计学意义(P>0.05)。在体通透性试验结果显示,EGCG组小鼠血清FITC-dextran水平低于Model组(P < 0.05),但高于WT组(P < 0.05);而肝脏和肠系膜淋巴结细菌移位率均低于Model组(P < 0.05),与WT组相比差异无统计学意义(P>0.05)。Western blotting分析显示,EGCG组小鼠肠黏膜组织p-JAK2和p-STAT3水平均低于Model组(P < 0.05),与WT组相比差异无统计学意义(P>0.05)。
      结论EGCG在体干预可以保护TNBS诱导的克罗恩病样肠道炎症,可能与保护肠屏障功能和抑制JAK2/STAT3炎症信号相关。

       

      Abstract:
      ObjectiveTo explore the effect and possible mechanism of epigallocatechin gallate (EGCG) on 2, 4, 6-trinitrobenzene sulfonic acid(TNBS)-induced colitis mice.
      MethodsTwenty-four male C57BL/6J mice were randomly divided into model group (Model group), control group(WT group) and EGCG intervention group(EGCG group).The colitis was induced with TNBS in Model group and EGCG group.After the model was successfully made, the EGCG group was intraperitoneally injected with 15 mg·kg-1·d-1 EGCG, and the WT group and Model group were given the same amount of 0.9% sodium chloride solution.After 4 weeks of intervention, HE staining, immunofluorescence, Western blotting, bacteria culture and so on were used to analyze the intestinal inflammation, levels of intestinal mucosa inflammation mediators, intestinal barrier structure and function, and changes of JAK2/STAT3 signal in intestinal mucosa.
      ResultsThe body mass gain of mice in EGCG group was higher than that in Model group(P < 0.05), and there was no significant difference compared with the WT group(P>0.05).At 3 to 4 weeks of intervention, the enteritis DAI score in EGCG group was significantly lower than that in Model group(P < 0.01).After 4 weeks of intervention, the intestinal inflammation scores, intestinal mucosa IL-6 and TNF-α levels of mice in EGCG group were lower than those in Model group(P < 0.05), but higher than those in WT group(P < 0.05);at the same time, the levels of intestinal epithelial tight junction proteins Occludin and ZO-1 were higher than those in Model group(P < 0.05), and there was no significant difference compared with the WT group(P>0.05).The results of in vivo permeability test showed that the serum FITC-dextran level in EGCG group was lower than that in Model group(P < 0.05), but higher than that in WT group(P < 0.05);while the proportion of bacterial translocation in liver and mesenteric lymph nodes was lower than that in Model group(P < 0.05), and there was no significant difference compared with the WT group(P>0.05).Western blotting analysis showed that the levels of p-JAK2 and p-STAT3 in the intestinal mucosa in EGCG group were lower than those in Model group(P < 0.05), and there was no significant difference compared with the WT group(P>0.05).
      ConclusionsEGCG intervention in vivo can protect TNBS-induced Crohn's disease-like intestinal inflammation, which may be related to the protection of intestinal barrier function and inhibition of JAK2/STAT3 inflammation signal.

       

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