电针通过GDNF/GFRα1/PI3K/Akt信号通路改善功能性消化不良大鼠胃肠运动

IF 1.5 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Current Medical Science Pub Date : 2025-08-01 Epub Date: 2025-08-08 DOI:10.1007/s11596-025-00086-4
Li Zhou, Xiao-Li Pan, De-Qian Yang, Qi Chen, Pai-di Xu, Hong-Xing Zhang
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引用次数: 0

摘要

目的:胃肠运动异常在功能性消化不良(FD)的发病机制中起重要作用。虽然电针(EA)在FD治疗中已证明有效,但其确切机制尚不清楚。本研究旨在阐明EA改善FD患者胃肠运动的具体机制。方法:采用体重、摄食量、胃肠蠕动、胃肠形态等生理指标对大鼠FD模型进行评价。在FD模型大鼠的经络点、非经络点和非腧穴处进行EA干预。采用胃肠动力试验指标,探讨EA对FD模型大鼠足三里(ST36)和太冲(LR3)胃肠动力的影响。采用Western blotting、实时荧光定量PCR、免疫荧光等技术,探讨EA改善FD模型大鼠胃肠运动的具体机制。结果:多因素应激干预可有效建立FD大鼠模型。ST36和LR3的EA显著改善了胃肠运动。此外,ST36和LR3的EA上调了胶质细胞系来源的神经营养因子(GDNF)、GDNF家族受体α1 (GFRα1)、磷脂酰肌醇3-激酶(PI3K)和蛋白激酶B (Akt)的蛋白表达,以及它们的mRNA表达水平和肠胶质细胞(EGCs)的数量。结论:EA能够通过激活GDNF/GFRα1/PI3K/Akt信号通路增加EGCs的数量,从而改善FD的胃肠运动。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Electroacupuncture Improves Gastrointestinal Motility in Rats with Functional Dyspepsia via the GDNF/GFRα1/PI3K/Akt Signaling Pathway.

Objective: Abnormal gastrointestinal motility plays a crucial role in the pathogenesis of functional dyspepsia (FD). Although electroacupuncture (EA) has demonstrated efficacy in FD treatment, its precise mechanism remains unclear. This study aimed to elucidate the specific mechanism through which EA improves gastrointestinal motility in FD.

Methods: Physiological indices, including body weight, food intake, gastrointestinal motility, and gastrointestinal morphology, were utilized to assess the FD model in rats. EA interventions were applied at meridian points, as well as non-meridian points and non-acupoints, in FD model rats. The effects of EA at zusanli (ST36) and taichong (LR3) on gastrointestinal motility in FD model rats were elucidated using gastrointestinal motility test indices. Techniques such as Western blotting, quantitative real-time PCR, and immunofluorescence were employed to determine the specific mechanisms by which EA improved gastrointestinal motility in FD model rats.

Results: Multifactorial stress intervention could be used to effectively establish an FD rat model. EA at ST36 and LR3 significantly improved gastrointestinal motility. Furthermore, EA at ST36 and LR3 upregulated the protein expression of glial cell line-derived neurotrophic factor (GDNF), GDNF family receptor alpha 1 (GFRα1), phosphatidylinositol 3-kinase (PI3K), and protein kinase B (Akt), along with their mRNA expression levels and the number of enteric glial cells (EGCs).

Conclusions: EA was capable of increasing the number of EGCs by activating the GDNF/GFRα1/PI3K/Akt signaling pathway, thereby improving gastrointestinal motility in FD.

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来源期刊
Current Medical Science
Current Medical Science Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
4.70
自引率
0.00%
发文量
126
期刊介绍: Current Medical Science provides a forum for peer-reviewed papers in the medical sciences, to promote academic exchange between Chinese researchers and doctors and their foreign counterparts. The journal covers the subjects of biomedicine such as physiology, biochemistry, molecular biology, pharmacology, pathology and pathophysiology, etc., and clinical research, such as surgery, internal medicine, obstetrics and gynecology, pediatrics and otorhinolaryngology etc. The articles appearing in Current Medical Science are mainly in English, with a very small number of its papers in German, to pay tribute to its German founder. This journal is the only medical periodical in Western languages sponsored by an educational institution located in the central part of China.
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