Fan Mingwei, Chen Tan, Tian Jinlan, Zhang Can, Zhao Zijian, Liu Xinru, Zhang Shuhui, Chen Yan
Binzhou Medical University, Binzhou, Shandong, China.
Binzhou Medical University, Binzhou, Shandong, China; Department of Gastroenterology, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Neuromodulation. 2025 Feb 14. doi: 10.1016/j.neurom.2024.12.006.
Although electroacupuncture (EA) at ST36 has been shown to alleviate visceral hypersensitivity in rats with ulcerative colitis (UC), the exact mechanism remains unknown. This study aims to investigate whether EA can effectively inhibit the activity of enteric glial cells (EGCs) through the adrenergic antiinflammatory pathway and thereby attenuate visceral hypersensitivity in rats with UC in remission.
Sprague-Dawley rats were continuously fed 5% dextran sulfate sodium (DSS) for seven days to establish intestinal inflammation. After seven days of remission, rats underwent EA (n = 6, 100 Hz, 1 mA, one hour) or sham EA (n = 6) for 14 days. A normal control group (n = 6) received no treatment. Inflammation was assessed using disease activity index (DAI) inflammatory cytokines. Visceral sensitivity was examined weekly by abdominal withdrawal reflexes (AWR) score. We used the enzyme-linked immunosorbent assay method to measure levels of norepinephrine (NE) in serum after EA. The expression of EGCs, levels of inflammatory cytokine S100 calcium-binding protein β (S100β), and associated pathway proteins receptor for advanced glycosylation end-products (RAGE), myeloid differentiation factor 88 (MyD88), and nuclear factor-κ B (NF-κB) in the colon were assessed using immunofluorescence staining and Western blotting.
The Model group exhibited elevated DAI scores, shortened colon, and increased inflammatory cytokines; the EA group showed significant relief of symptoms. The Model group exhibited elevated visceral hypersensitivity, which resolved after 14 days of EA treatment. The EA group exhibited higher NE levels than did the Model group. Compared with the Model group, the expression of EGCs in the colonic submucosa was reduced in the EA group, and the expression of S100β, RAGE, MyD88, and NF-κB proteins were downregulated.
This study suggests that EA potentially reduces visceral hypersensitivity in UC by decreasing the activity of EGCs and the release of S100β through noradrenergic pathway.
尽管已证明电针足三里穴可减轻溃疡性结肠炎（UC）大鼠的内脏超敏反应，但其确切机制仍不清楚。本研究旨在探讨电针是否能通过肾上腺素能抗炎途径有效抑制肠胶质细胞（EGC）的活性，从而减轻缓解期UC大鼠的内脏超敏反应。
将Sprague-Dawley大鼠连续7天喂食5%葡聚糖硫酸钠（DSS）以建立肠道炎症。缓解7天后，大鼠接受电针治疗（n = 6，100 Hz，1 mA，1小时）或假电针治疗（n = 6），持续14天。正常对照组（n = 6）不接受治疗。使用疾病活动指数（DAI）炎症细胞因子评估炎症。每周通过腹部退缩反射（AWR）评分检查内脏敏感性。我们采用酶联免疫吸附测定法测量电针后血清中去甲肾上腺素（NE）的水平。使用免疫荧光染色和蛋白质印迹法评估结肠中EGC的表达、炎症细胞因子S100钙结合蛋白β（S100β）的水平以及相关途径蛋白晚期糖基化终产物受体（RAGE）、髓样分化因子88（MyD88）和核因子κB（NF-κB）。
模型组DAI评分升高、结肠缩短且炎症细胞因子增加；电针组症状明显缓解。模型组表现出内脏超敏反应升高，电针治疗14天后缓解。电针组NE水平高于模型组。与模型组相比，电针组结肠黏膜下层EGC的表达降低，S100β、RAGE、MyD88和NF-κB蛋白的表达下调。
本研究表明，电针可能通过去甲肾上腺素能途径降低EGC的活性和S100β的释放，从而降低UC大鼠的内脏超敏反应。
