Basic Study
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 7, 2025; 31(21): 107395
Published online Jun 7, 2025. doi: 10.3748/wjg.v31.i21.107395
Electroacupuncture at ST36 ameliorates gastric dysmotility in rats with diabetic gastroparesis via the nucleus tractus solitarius-vagal axis
You Zhang, Yi-Wen Tang, Jin Zhou, Yan-Rong Wei, Yu-Ting Peng, Zi Yan, Zeng-Hui Yue
You Zhang, Yi-Wen Tang, Jin Zhou, Yan-Rong Wei, Yu-Ting Peng, Zi Yan, Zeng-Hui Yue, College of Acupuncture, Massage and Rehabilitation, Hunan University of Chinese Medicine, Changsha 410208, Hunan Province, China
Author contributions: Zhang Y and Yue ZH designed the study; Zhang Y, Tang YW and Zhou J performed the experiments; Tang YW, Zhou J, Wei YR, Peng YT and Yan Z conducted a survey and search; Zhang Y analyzed the results and wrote the article; All authors read and approved the final version.
Supported by the Natural Science Foundation of Hunan Province, China, No. 2023JJ30462; Hunan Provincial Department of Science and Technology, No. 2023SK2045, No. 22JBZ007 and No. Z2023JB01; and Graduate Research and Innovation Projects of Hunan Province, No. 2024CX031.
Institutional review board statement: This study does not involve any human experiments.
Institutional animal care and use committee statement: All animal studies were approved by the Medical Ethics Committee of Hunan University of Traditional Chinese Medicine (No. HNUCM21-2311-08).
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zeng-Hui Yue, FACE, College of Acupuncture, Massage and Rehabilitation, Hunan University of Chinese Medicine, No. 300 Bachelor Road, Yuelu District, Changsha 410208, Hunan Province, China. yue5381316@126.com
Received: March 23, 2025
Revised: April 11, 2025
Accepted: May 23, 2025
Published online: June 7, 2025
Processing time: 75 Days and 23.9 Hours
Abstract
BACKGROUND

Diabetic gastroparesis (DGP), characterized by delayed gastric emptying and impaired motility, poses significant therapeutic challenges due to its complex neural and molecular pathophysiology. Emerging evidence suggests that electroacupuncture (EA) at ST36 modulates gastrointestinal function; however, the precise neuromolecular pathways underlying its efficacy in DGP remain incompletely defined.

AIM

To elucidate the neural mechanisms underlying EA at ST36 improving DGP gastric motility through the nucleus tractus solitarius (NTS)-vagal axis.

METHODS

The DGP model was established via a single high-dose intraperitoneal injection of 2% streptozotocin combined with an 8-week high-sugar/high-fat diet. Interventions included EA at ST36, pharmacological modulation [choline acetyltransferase (ChAT) agonist polygalacic acid (PA) and inhibitor antagonist alpha-NETA], and subdiaphragmatic vagotomy. Post-intervention observations included body weight and blood glucose levels. Gastric emptying was evaluated using phenol red assays, gastric slow-wave recordings, and dynamic positron emission tomography-computed tomography imaging. Histopathological analysis (hematoxylin-eosin staining) and molecular assessments (Western blot, immunofluorescence) were performed to quantify gastric smooth muscle-associated factors [neuronal nitric oxide synthase (nNOS), cluster of differentiation 117 (C-kit), stem cell factor (SCF)] and vagal targets [ChAT, α7 nicotinic acetylcholine receptor (α7nAChR)] in the ST36 acupoint region, L4-L6 spinal segments, and NTS. Gastrointestinal peptides [gastrin (Gas), motilin (MLT) and vasoactive intestinal peptide (VIP)] were measured via enzyme-linked immunosorbent assay.

RESULTS

The study found that EA significantly increased the rate of gastric emptying, restored the slow-wave rhythms of the stomach, and improved the architecture of the smooth muscles in the stomach. This was evidenced by a reduction in inflammatory infiltration and an increase in the expression of nNOS, C-kit, and SCF. Mechanistically, EA activated vagal targets (ChAT and α7nAChR) at ST36, transmitting signals via spinal segments L4-L6 to the NTS, subsequently regulating gastrointestinal peptides (Gas, MLT, VIP) and restoring interstitial cells of Cajal (ICCs) function via subdiaphragmatic vagal efferent pathways. It is crucial to note that subdiaphragmatic vagotomy led to the abrogation of EA-induced enhancements in gastric motility and ICC recovery, thereby confirming the indispensable role of vagal efferent signalling.

CONCLUSION

EA provides a novel molecular mechanism for improving gastrointestinal motility in DGP via a peripheral stimulation (ST36), spinal afferent (L4-L6), brainstem integration (NTS), vagal efferent (gastric) circuit.

Keywords: Electroacupuncture; Diabetic gastroparesis; Vagus nerve; Gastric motility; Interstitial cells of Cajal; Positron emission tomography-computed tomography imaging

Core Tip: Multimodal validation: Electroacupuncture (EA) significantly enhanced gastric emptying (validated by positron emission tomography-computed tomography), restored gastric slow-wave rhythms, and improved smooth muscle architecture via upregulation of neuronal nitric oxide synthase, cluster of differentiation 117, stem cell factor. Mechanistic insight: EA activates cholinergic targets (choline acetyltransferas/α7 nicotinic acetylcholine receptor) at ST36, transmits signals via spinal L4-L6 afferents to the nucleus tractus solitarius, and modulates gastrointestinal peptides (ghrelin, motilin, vasoactive intestinal peptide) through subdiaphragmatic vagal efferent, ultimately restoring interstitial cells of Cajal function. Translational relevance: Subdiaphragmatic vagotomy abolished EA’s therapeutic effects, unequivocally establishing vagal efferent signaling as indispensable.