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电针通过GDNF/GFRα1/PI3K/Akt信号通路改善功能性消化不良大鼠的胃肠动力。

Electroacupuncture Improves Gastrointestinal Motility in Rats with Functional Dyspepsia via the GDNF/GFRα1/PI3K/Akt Signaling Pathway.

作者信息

Zhou Li, Pan Xiao-Li, Yang De-Qian, Chen Qi, Xu Pai-di, Zhang Hong-Xing

机构信息

Institute of Acupuncture and Moxibustion, Jianghan University, Wuhan, 430056, China.

College of Traditional Chinese Medicine, School of Medicine, Jianghan University, Wuhan, 430056, China.

出版信息

Curr Med Sci. 2025 Aug 8. doi: 10.1007/s11596-025-00086-4.

Abstract

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.

摘要

目的

胃肠动力异常在功能性消化不良(FD)的发病机制中起关键作用。尽管电针(EA)已证明对FD治疗有效,但其确切机制仍不清楚。本研究旨在阐明EA改善FD患者胃肠动力的具体机制。

方法

利用包括体重、食物摄入量、胃肠动力和胃肠形态在内的生理指标评估大鼠的FD模型。对FD模型大鼠的经络穴位、非经络穴位和非穴位进行EA干预。利用胃肠动力测试指标阐明足三里(ST36)和太冲(LR3)穴位电针对FD模型大鼠胃肠动力的影响。采用蛋白质印迹法、定量实时聚合酶链反应和免疫荧光等技术确定EA改善FD模型大鼠胃肠动力的具体机制。

结果

多因素应激干预可有效建立FD大鼠模型。ST36和LR3穴位电针显著改善胃肠动力。此外,ST36和LR3穴位电针上调了胶质细胞源性神经营养因子(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(EGC)数量。

结论

电针能够通过激活GDNF/GFRα1/PI3K/Akt信号通路增加肠胶质细胞数量,从而改善功能性消化不良患者的胃肠动力。

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