Liu Geng-Hao, Liu Hsuan-Miao, Chen Yu-Sheng, Lee Tzung-Yan
Division of Acupuncture and Moxibustion, Department of Traditional Chinese Medicine, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan.
Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Evid Based Complement Alternat Med. 2020 Apr 27;2020:2087903. doi: 10.1155/2020/2087903. eCollection 2020.
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.
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.
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-, TNF-, and IL-6, but decreased adiponectin. These changes were reversed by EA, accompanied by modulation of the overall structure of gut microbiota.
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.
炎症性肠病与肠道微生物群之间的关系密不可分。电针（EA）可缓解急性实验性结肠炎，但肠道微生物的表现及机制仍未完全明确。我们研究了电针与肠道微生物之间的关系，并阐明紧密连接和脂联素在电针抗炎作用中的作用。
将雄性C57BL/6小鼠随机分为三组：正常对照组、葡聚糖硫酸钠（DSS）诱导的溃疡性结肠炎组（DSS）和电针足三里（ST36）的DSS组（DSS + EA）。评估小鼠体重、疾病活动指数（DAI）评分、结肠长度和组织学评分以确定结肠炎的严重程度。通过免疫组织化学（IHC）方法检测结肠炎症和紧密连接。通过多重免疫测定法检测血浆细胞因子和脂联素以确认全身反应。通过16S rRNA基因测序进行肠道微生物群分析。
电针有助于缓解宏观和微观层面的结肠炎症。它可以降低疾病活动度，维持结肠长度，并改善组织学炎症反应。在免疫组织化学染色中，电针降低了CD11b、F4/80、TLR4和MyD88的表达，并保留了claudin-1和ZO-1的表达。与对照组相比，DSS组的CRP、IFN-、TNF-和IL-6水平升高，但脂联素水平降低。这些变化被电针逆转，同时伴随着肠道微生物群整体结构的调节。
我们的研究结果表明，电针通过MyD88依赖途径的TLR4信号传导发挥其治疗作用。电针可以增加脂联素，维持粘膜紧密连接，并调节肠道微生物群。
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