Mingwei Fan, Tan Chen, Jinlan Tian, Can Zhang, Zijian Zhao, Xinru Liu, Shuhui Zhang, Yan Chen
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引用次数: 0
Abstract
Background and aims: 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.
Materials and methods: 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.
Results: 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.
Conclusion: 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.
期刊介绍：
Neuromodulation: Technology at the Neural Interface is the preeminent journal in the area of neuromodulation, providing our readership with the state of the art clinical, translational, and basic science research in the field. For clinicians, engineers, scientists and members of the biotechnology industry alike, Neuromodulation provides timely and rigorously peer-reviewed articles on the technology, science, and clinical application of devices that interface with the nervous system to treat disease and improve function.
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