Electroacupuncture-Regulated Bile Acid Metabolism and Farnesoid X Receptor Expression in Constipation-Predominant Irritable Bowel Syndrome Rat: A Preclinical Study

胆汁酸 法尼甾体X受体 电针 G蛋白偶联胆汁酸受体 新陈代谢 内科学 内分泌学 信号转导 化学 蛋白质表达 药理学 胆汁酸吸收不良 FGF19型 牛磺胆酸 下调和上调 医学 基因表达 生物 药物代谢
作者
Shiyuan Jiang,Xiaoyu Wang,Qu Zhang,Jing Guo,Xiaoyu LIU,Yangshuai Su,XiangHong Jing,JianHua Sun,Lixia Pei
出处
期刊:Digestion [Karger Publishers]
卷期号:: 1-14
标识
DOI:10.1159/000550560
摘要

INTRODUCTION: The efficacy of electroacupuncture (EA) treatment in alleviating visceral hypersensitivity with irritable bowel syndrome (IBS) has been established. Abnormal bile acid metabolism and farnesoid X receptor (FXR) expression are recognized as potential contributors to visceral hypersensitivity in IBS. This study as a preclinical study of IBS visceral hypersensitivity explored the potential of EA to reduce visceral hypersensitivity in rats with IBS by improving bile acid metabolism and FXR expression. METHODS: Heterotypic intermittent stress (HIS) for 9 days was used to induce visceral hypersensitivity in constipation-predominant irritable bowel syndrome (IBS-C). EA/sham EA bilateral ST36 and LR3 acupoints began on the 5th day of HIS. Electromyography of the abdominal external oblique muscle and calcitonin gene-related peptide were used to assess colonic hypersensitivity. Colonoscopy and histopathological examination were used to evaluate pathological changes in the colon. Bile acid composition was analyzed using high-performance liquid chromatography-mass spectrometry, while FXR expression in colon tissue was quantified through immunofluorescence and Western blot. RESULTS: HIS induced visceral hypersensitivity in IBS-C rats. EA not only regulated bile acid levels in the feces of IBS-C rats, but also had a downregulatory effect on the overexpression of FXR in the colon tissue of rats with IBS-C. The therapeutic effects were better than those of the sham EA. EA treatment alleviated visceral hypersensitivity in the colon of IBS-C rats. CONCLUSION: Our data suggested that EA normalized colonic bile acid signaling and FXR protein expression in an IBS-C rat model, offering a mechanistic hypothesis for future clinical evaluation.
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