MedElevator
Войти в исследования Neuroreport · 2025
Electroacupuncture at Huantiao (GB30) and Zusanli (ST36) acupoints promotes peripheral nerve regeneration by enhancing energy metabolism in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ji Qingjie, Zhang Nannan, Zhang Baojuan, Chen Yunfeng, Zhang Qingqing, Yao Xiaoying, Zhang Meimei, Zheng Qian, Ni Guangxia, Shan Fangzhen
Аннотация
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.
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.