{"title":"Electroacupuncture at Huantiao (GB30) and Zusanli (ST36) acupoints promotes peripheral nerve regeneration by enhancing energy metabolism in mice.","authors":"Qingjie Ji, Nannan Zhang, Baojuan Zhang, Yunfeng Chen, Qingqing Zhang, Xiaoying Yao, Meimei Zhang, Qian Zheng, Guangxia Ni, Fangzhen Shan","doi":"10.1097/WNR.0000000000002209","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Peripheral nerve injury (PNI) leads to substantial functional impairment, yet current therapies remain limited. Electroacupuncture (EA) is a promising intervention for PNI, but its mechanisms, particularly its role in modulating energy metabolism during nerve regeneration, are poorly understood.</p><p><strong>Methods: </strong>A mouse PNI model was established by crushing the right sciatic nerve. EA stimulation was applied on the right side acupoints of Huantiao (GB30) and Zusanli (ST36) in PNI mice. Hind-limb splaying and gait analysis were used to evaluate motor function, and electrophysiological tests were used to assess nerve conduction. Nerve regeneration and molecular mechanisms were examined by Western blot, immunofluorescence, and transmission electron microscopy.</p><p><strong>Results: </strong>We found that EA treatment significantly improved motor function, increased compound muscle action potential amplitude, and reduced muscle atrophy. Axonal regeneration was accelerated, as evidenced by increased SCG10-positive fibers. EA increased mitochondrial transcription factor A, mitochondrial DNA copy number, and mitochondrial electron transport chain activity, indicative of improved mitochondrial function and oxidative phosphorylation. Moreover, EA was identified to enhance energy metabolism by upregulating neurotrophic factors and modulating the AMPK/mTOR/p70S6K pathway.</p><p><strong>Conclusion: </strong>Our findings indicate that EA at Huantiao (GB30) and Zusanli (ST36) promotes nerve regeneration and functional recovery after PNI by upregulating energy metabolism. This study provides a novel perspective on the therapeutic potential of EA in peripheral nerve repair.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 14","pages":"874-885"},"PeriodicalIF":1.7000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroreport","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/WNR.0000000000002209","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/8/4 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Peripheral nerve injury (PNI) leads to substantial functional impairment, yet current therapies remain limited. Electroacupuncture (EA) is a promising intervention for PNI, but its mechanisms, particularly its role in modulating energy metabolism during nerve regeneration, are poorly understood.
Methods: A mouse PNI model was established by crushing the right sciatic nerve. EA stimulation was applied on the right side acupoints of Huantiao (GB30) and Zusanli (ST36) in PNI mice. Hind-limb splaying and gait analysis were used to evaluate motor function, and electrophysiological tests were used to assess nerve conduction. Nerve regeneration and molecular mechanisms were examined by Western blot, immunofluorescence, and transmission electron microscopy.
Results: We found that EA treatment significantly improved motor function, increased compound muscle action potential amplitude, and reduced muscle atrophy. Axonal regeneration was accelerated, as evidenced by increased SCG10-positive fibers. EA increased mitochondrial transcription factor A, mitochondrial DNA copy number, and mitochondrial electron transport chain activity, indicative of improved mitochondrial function and oxidative phosphorylation. Moreover, EA was identified to enhance energy metabolism by upregulating neurotrophic factors and modulating the AMPK/mTOR/p70S6K pathway.
Conclusion: Our findings indicate that EA at Huantiao (GB30) and Zusanli (ST36) promotes nerve regeneration and functional recovery after PNI by upregulating energy metabolism. This study provides a novel perspective on the therapeutic potential of EA in peripheral nerve repair.
期刊介绍：
NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool.
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