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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Effect of Electroacupuncture in Mice with Dextran Sulfate Sodium-Induced Colitis and the Influence of Gut Microbiota
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Effect of Electroacupuncture in Mice with Dextran Sulfate Sodium-Induced Colitis and the Influence of Gut Microbiota

机译:电针对葡聚糖硫酸钠诱导的结肠炎的电针对小鼠的影响及肠道微生物的影响

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摘要

Background. The relationship between inflammatory bowel disease and gut microbiota is inextricable. Electroacupuncture (EA) can alleviate acute experimental colitis, but the performance of intestinal microorganisms and the mechanism are still not fully understood. We investigated the relationship between the EA and gut microbes and clarified the role of tight junction and adiponectin in the anti-inflammatory effect of EA. Methods. Male C57BL/6 mice were randomized into three groups: normal control, dextran sulfate sodium- (DSS-) induced ulcerative colitis (DSS), and DSS with EA ST36 (DSS?+?EA). Mice body weight, DAI score, colon length, and histological score were evaluated for colitis severity. Colonic inflammation and tight junctions were demonstrated by the immunohistochemical (IHC) method. Systemic responses were confirmed by plasma cytokines and adiponectin with multiplex immunoassays. Gut microbiome profiling was conducted by 16S rRNA gene sequencing. Results. EA had benefit in relieving both macroscopic and microscopic colonic inflammation. It can reduce disease activity, maintain colon length, and ameliorate histological inflammatory reaction. In IHC stain, EA decreased CD11b, F4/80, TLR4, and MyD88 and preserved claudin-1 and ZO-1 expression. Compared with the control group, the DSS group showed elevated levels of CRP, IFN-γ, TNF-α, and IL-6, but decreased adiponectin. These changes were reversed by EA, accompanied by modulation of the overall structure of gut microbiota. Conclusion. Our findings suggest that EA exerts its therapeutic effect by TLR4 signaling via the MyD88-dependent pathway. EA could increase adiponectin, maintain mucosal tight junctions, and modulate gut microbiota.
机译:背景。炎症性肠病和肠道微生物植物之间的关系是密切的。电针(EA)可以缓解急性实验性结肠炎,但肠道微生物的性能和机制仍然没有完全理解。我们调查了EA和肠道微生物之间的关系,并阐明了紧密结和脂联素在EA抗炎作用中的作用。方法。将雄性C57BL / 6小鼠随机分为三组:正常对照,葡聚糖硫酸钠 - (DSS-)诱导的溃疡性结肠炎(DSS),以及具有EA ST36的DSS(DSS?+ ea)。对小鼠体重,傣族分数,结肠长度和组织学分数进行结肠炎严重程度。通过免疫组织化学(IHC)方法证明了结肠炎症和紧密交界。通过血浆细胞因子和脂联素与多重免疫测定蛋白确认系统响应。肠道微生物谱分析由16S rRNA基因测序进行。结果。 EA有益处缓解宏观和微观结肠炎症。它可以减少疾病活动,维持结肠长度和改善组织学炎症反应。在IHC染色中,EA降低CD11B,F4 / 80,TLR4和MYD88,并保存克劳德蛋白-1和ZO-1表达。与对照组相比,DSS组显示CRP,IFN-γ,TNF-α和IL-6水平升高,但脂联素降低。通过EA逆转这些变化,伴随着肠道微生物肿的整体结构的调节。结论。我们的研究结果表明,EA通过MyD88依赖途径通过TLR4信号传导施加其治疗效果。 EA可以增加脂联素,维持粘膜紧密连接,并调节肠道微生物。

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