DOI 10.1080/01616412.2025.2553149
Electroacupuncture combined with botulinum toxin type A promotes common peroneal nerve repair and activation of GDNF-BDNF/TrkB signaling pathway in post-stroke limb spasticity rats.
Аннотация
BACKGROUND
Post-stroke limb spasticity (PSLS) is a rehabilitation problem that needs to be solved urgently, electroacupuncture (EA), a safe and effective adjunctive rehabilitation therapy with relatively few side effects, and botulinum toxin type A (BTX-A) can improve motor function; however, it is not clear whether EA combined with BTX-A is more effective in improving PSLS. This study will investigate the effects and mechanisms of EA combined with BTX-A to improve PSLS in rats.
METHODS
PSLS rat model was prepared and treated with EA, BTX-A, or EA+BTX-A, Zea longa, modified Ashworth, and modified neurological severity score to assess the changes of neurological function and dystonia, and to observe the cerebral infarction condition, fibers changes of gastrocnemius muscle, common peroneal nerve pathology morphology, changes of neural repair factors and GDNF/BDNF/TrkB signaling pathway in the rats, respectively.
RESULTS
The results showed that EA combined with BTX-A effectively promotes the recovery of neurological function in rats with post-stroke limb spasticity, improves axonal and myelin regeneration of the gastrocnemius nerve on the operated side, promotes the repair of the common peroneal nerve, and activates the GDNF-BDNF/TrkB signaling pathway.
CONCLUSIONS
Collectively, EA combined with BTX-A for the treatment of PSLS may be associated with the promotion of common peroneal nerve repair and modulation of the GDNF-BDNF/TrkB signaling pathway.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
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.
Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.