Aims

Electroacupuncture (EA) at ST36 has been verified to ameliorate experimental acute colitis. However, the effect of EA on chronic colitis and its mechanism has not yet been explored. This study aimed to assess the protective effect of EA against chronic colitis and the related mechanisms.

Main methods

Chronic colitis was induced by dextran sulfate sodium (DSS) in C57BL/6 mice, and EA was applied throughout the entire experiment. Colonic inflammation and intestinal barrier integrity were evaluated. Alterations in the gut microbiota were analyzed by 16S rRNA gene sequencing. The fecal microbiota transplantation (FMT) experiment was used to further confirm the effect of the gut microbiota on the barrier protective effect of EA. The potential molecular mechanisms were explored by western blotting.

Key findings

(1) EA lowered the disease activity index (DAI) and histological scores, decreased the levels of TNFα, IL1β, IL6 and iNOS, and increased the IL10 level in DSS-induced chronic colitis. (2) EA upregulated the protein expression of ZO-1, Occludin, E-Cadherin and mucin2 (MUC2), reduced the apoptosis and proliferation of intestinal epithelial cells (IECs) and intestinal permeability. (3) EA enhanced the gut microbiota diversity and restored the community structure. (4) Both the low-frequency EA (LEA) FMT and high-frequency EA (HEA) FMT maintained the intestinal barrier integrity. (5) EA promoted activation of the mitogen activated protein kinase (MAPK) signaling pathway.

Significance

EA can relieve chronic experimental colitis, and this effect may depend on activation of the MAPK signaling pathway through modulation of the gut microbiota to preserve the intestinal barrier.

中文翻译：

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电针通过调节DSS诱发的慢性结肠炎中的肠道菌群来维持肠道屏障的完整性

目的

已证实ST36的电针（EA）可改善实验性急性结肠炎。但是，尚未探讨EA对慢性结肠炎的作用及其机制。这项研究旨在评估EA对慢性结肠炎的保护作用及其相关机制。

主要方法

硫酸葡聚糖硫酸钠（DSS）在C57BL / 6小鼠中诱发慢性结肠炎，并且在整个实验过程中均采用EA。评估结肠炎症和肠屏障完整性。通过16S rRNA基因测序分析肠道菌群的变化。粪便菌群移植（FMT）实验用于进一步证实肠道菌群对EA的屏障保护作用的影响。通过蛋白质印迹探索了潜在的分子机制。

主要发现

（1）EA降低了DSS所致慢性结肠炎的疾病活动指数（DAI）和组织学评分，降低了TNFα，IL1β，IL6和iNOS的水平，并增加了IL10的水平。（2）EA上调ZO-1，Occludin，E-Cadherin和mucin2（MUC2）的蛋白表达，降低肠上皮细胞（IECs）的凋亡和增殖以及肠通透性。（3）EA增强了肠道菌群多样性，恢复了群落结构。（4）低频EA（LEA）FMT和高频EA（HEA）FMT都能保持肠屏障的完整性。（5）EA促进了有丝分裂原活化蛋白激酶（MAPK）信号通路的激活。

意义

EA可以缓解慢性实验性结肠炎，这种作用可能取决于通过调节肠道菌群以保留肠道屏障来激活MAPK信号通路。