Effect of Electroacupuncture in Mice with Dextran Sulfate Sodium-Induced Colitis and the Influence of Gut Microbiota

Geng-Hao Liu; Hsuan-Miao Liu; Yu-Sheng Chen; Tzung-Yan Lee

doi:10.1155/2020/2087903

Effect of Electroacupuncture in Mice with Dextran Sulfate Sodium-Induced Colitis and the Influence of Gut Microbiota

Evid Based Complement Alternat Med. 2020 Apr 27:2020:2087903. doi: 10.1155/2020/2087903. eCollection 2020.

Authors

Geng-Hao Liu^{1

2

3

4}, Hsuan-Miao Liu⁵, Yu-Sheng Chen¹, Tzung-Yan Lee^{5

6}

Affiliations

¹ Division of Acupuncture and Moxibustion, Department of Traditional Chinese Medicine, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan.
² Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
³ School of Traditional Chinese Medicine, Chang Gung University, Taoyuan, Taiwan.
⁴ Sleep Center, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
⁵ Graduate Institute of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
⁶ Department of Traditional Chinese Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan.

Abstract

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.