Shiyuan Jiang, Lixia Pei, Lu Chen, Jianhua Sun, Yafang Song
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引用次数: 0
摘要
导言:感染后肠易激综合征(PI-IBS)是一种在急性胃肠道感染后出现的功能性肠病。电针(EA)可以调节肠道微生物群,缓解内脏超敏反应。胶质细胞源性神经营养因子(GDNF)是内脏超敏反应的潜在因素。本研究旨在探讨 EA 是否能通过 GDNF 信号调节肠道微生物群来减轻 PI-IBS 的内脏超敏反应。方法:使用 2,4,6-三硝基苯磺酸(TNBS)诱导 PI-IBS 小鼠的内脏超敏反应。使用腹部退缩反射(CRD)评估肠道内脏敏感性。对肠道微生物群落进行 16S 核糖体 RNA(16S rRNA)测序:结果:与模型组相比,GDNF能加剧肠道微生物群的失衡,并增加内脏超敏性。而 EA 治疗可增加肠道微生物群的丰富性和多样性,减少物种间的差异,减轻内脏敏感性:结论:EA可通过GDNF信号调节肠道微生物群来缓解PI-IBS的内脏超敏反应,为EA治疗PI-IBS的机理研究提供了新的思路。
Mechanisms of Electroacupuncture in Alleviating Visceral Hypersensitivity in Post-Infectious Irritable Bowel Syndrome Mice: The Role of GDNF Signaling Pathway and Gut Microbiota.
Introduction: Post-infectious irritable bowel syndrome (PI-IBS) is a functional bowel disease that develops following an acute gastrointestinal infection. Electroacupuncture (EA) can regulate the gut microbiota and alleviate visceral hypersensitivity. Glial cell-derived neurotrophic factor (GDNF) is a potential factor in visceral hypersensitivity reactions. The aim of this study was to explore whether EA could alleviate visceral hypersensitivity in PI-IBS by regulating gut microbiota through GDNF signaling.
Methods: 2,4,6-trinitrobenzene sulfonic acid was used to induce visceral hypersensitivity in PI-IBS mice. Intestinal visceral sensitivity was assessed by using the abdominal withdrawal reflex (colorectal distention). 16S ribosomal RNA sequencing profiles the gut microbiome community.
Results: GDNF can exacerbate the imbalances of the gut microbiota and increase visceral hypersensitivity compared with the model group. Whereas EA treatment increases the richness and diversity of the gut microbiota, decreases differences among species and alleviates visceral sensitivity.
Conclusion: EA can alleviate visceral hypersensitivity in PI-IBS by regulating the gut microbiota via GDNF signaling, providing new insights for mechanistic research on EA in PI-IBS treatment.