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Research Article | Open Access

Electroacupuncture reduces calcium influx and inhibits endoplasmic reticulum stress by inhibiting the PKCδ-TRPA1 pathway to promote motor function recovery after spinal cord injury

Yihui Zhang1,‡( ), Chenhe Liang1,2,‡, Zhiyang Huang3,4,‡, Yusi Hu5,‡, Yujun Mo3,4,‡, Shaoxia Ning6, Ziyi Li6, Yungang Wu1, Jiaxin Zhang1, Xiaokun Li4( ), Zhouguang Wang1,3,4 ( )
Department of Traditional Chinese Orthopaedics, the First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang Street, Wenzhou City, Zhejiang Province 325035, China
The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang Street, Wenzhou City, Zhejiang Province 325035, China
Wound Healing Center, the First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang Street, Wenzhou City, Zhejiang Province 325035, China
National Key Laboratory of Macromolecular Drug Development and Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Chashan Street, Wenzhou City, Zhejiang Province 325035, China
Alberta Institute, Wenzhou Medical University, Wenzhou, Chashan Street, Wenzhou City, Zhejiang Province 325035, China
Cixi Biomedical Research Institute, Wenzhou Medical University, No. 999, South Second Ring Road East, Hushan Street, Cixi City, Ningbo City, Zhejiang Province 315300, China

‡Yihui Zhang, Chenhe Liang, Zhiyang Huang, Yusi Hu, and Yujun Mo contributed equally.

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Highlights

• The activation of PKCδ-TRPA1 induced by mechanical injury and the inflammatory microenvironment after SCI is a significant cause of neuronal calcium overload, which subsequently leads to ER stress and apoptosis.

• EA stimulation at the Shen Shu points can reduce the expression of PKCδ-TRPA1 and alleviate ER stress and apoptosis induced by neuronal calcium overload.

• Stimulation of the Shen Shu points by EA promoted neurogenesis and axon elongation by enhancing the secretion of neurotrophic factors and stabilizing microtubules, thereby facilitating the recovery of motor function in SCI mice.

Abstract

Background

Following spinal cord injury (SCI), mechanical trauma and an inflammatory microenvironment activate the PKCδ-TRPA1 pathway, resulting in calcium overload within neurons and subsequently inducing endoplasmic reticulum (ER) stress–mediated neuronal apoptosis. The mechanisms and therapeutic potential of electroacupuncture (EA) in the treatment of SCI have yet to be fully elucidated. This study aimed to explore the causes of neuronal Ca2+ overload post-SCI and to investigate the neuroprotective and regenerative mechanisms of EA in an SCI mouse model.

Methods

C57BL6 mice were randomly divided into a Sham group, an SCI group, and an SCI + EA group. The Basso Mouse Scale, motor-evoked potential, and movement videos of the mice were captured, and DeepLabCut was used to analyze the recovery of motor function. Western blotting was used to detect the protein levels of related indicators. Immunofluorescence staining was used to analyse the cellular localization and fluorescence intensity of each indicator. Hematoxylin and eosin staining and Nissl staining were used for histological evaluation. EA treatment resulted in higher BMS scores; increased ankle, knee, and hip mobility; and improved hindlimb support in the EA group.

Results

PKCδ and TRPA1 protein expression was upregulated after SCI, and neuronal calcium ion overload occurred, leading to neuronal ER stress–induced apoptosis. After EA treatment, inflammatory microenvironment-related indicators were downregulated, which inhibited the activation of calcium channels by PKCδ-TRPA1, reduced ER stress–induced apoptosis caused by calcium overload in neurons, and protected neurons from secondary injury. EA increases the expression of neurotrophic factors and promotes nerve regeneration, and we found that EA treatment promotes axonal elongation by stabilizing microtubules.

Conclusions

According to our findings, (ⅰ) mechanical injury and the inflammatory microenvironment after SCI activate PKCδ-TRPA1, which is important for neuronal ER stress and apoptosis caused by neuronal calcium overload. (ⅱ) EA treatment reduces the expression of PKCδ-TRPA1 as well as the ER stress and apoptosis caused by neuronal calcium overload. (ⅲ) EA promoted neurogenesis and axonal regeneration by promoting the secretion of neurotrophic factors and promoted axon elongation by stabilizing microtubules, thus promoting the recovery of motor function in SCI mice.

Graphical Abstract

Keywords

Spinal cord injuryElectroacupuncturePKCδ/TRPA1Endoplasmic reticulum stressNeurogenesis

References

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Burns & Trauma
Volume 14 Issue 2,
March 2026
DOI: 10.1093/burnst/tkaf066

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Zhang Y, Liang C, Huang Z, et al. Electroacupuncture reduces calcium influx and inhibits endoplasmic reticulum stress by inhibiting the PKCδ-TRPA1 pathway to promote motor function recovery after spinal cord injury. Burns & Trauma, 2026, 14(2). https://doi.org/10.1093/burnst/tkaf066

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Received: 23 March 2025
Revised: 20 September 2025
Accepted: 15 October 2025
Published: 24 October 2025
© The Author(s) 2025. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.