Electroacupuncture improves motor function after ischemic stroke via regulating mitochondrial dynamics

电针 医学 运动功能 缺血性中风 动力学(音乐) 线粒体 功能(生物学) 神经科学 内科学 缺血 大鼠模型 心脏病学 冲程(发动机) 新陈代谢 缺血性损伤 膜电位 碳水化合物代谢 电动机控制 脑缺血 物理医学与康复 麻醉 运动活动
作者
Zuanfang Li,Ji Xinru,Xiuxiu Wang,Jiawei Wang,Ruhui Lin,Xiaohan Ma,Qingqing Zhang,Liang Shengxiang
出处
期刊:Brain Research Bulletin [Elsevier BV]
卷期号:232: 111599-111599 被引量:4
标识
DOI:10.1016/j.brainresbull.2025.111599
摘要

OBJECTIVE: Previous studies have demonstrated that electroacupuncture (EA) exerts a protective effect in middle cerebral artery occlusion (MCAO) rats and may improve motor function, but the specific mechanism involved remains to be elucidated. This study aimed to further investigate the effects of EA at the Quchi (LI11) and Zusanli (ST36) acupoints on ischemic stroke motor function and the underlying mechanism. METHODS: Following the establishment of MCAO model, the rats in EA group were treated at LI11 and ST36 acupoints. Catwalk gait analysis was used to assess ethology. T2 weighted imaging was used to assess cerebral infarct volume. H&E and Nissl staining was used to assess cortical morphology. Glucose metabolism was detected by chemical exchange saturation transfer (CEST). Chemiluminescence was used to detect the cortical adenosine triphosphate (ATP). Mitochondrial morphological changes were observed by transmission electron microscopy(TEM). The protein and mRNA expressions of mitochondrial dynamics related genes Drp1, Fis1, Mfn2, Mfn1 and Opa1 were detected by western blot and qPCR respectively. RESULTS: EA intervention improved gait dynamics, reduced cerebral infarct volume, ameliorated cortical pathological morphological changes and neuronal loss. EA significantly alleviated mitochondrial morphological changes. EA improved mitochondrial dynamic disorder by significantly increasing the expression of Opa1 and inhibiting the expression of Drp1, thus improving glucose metabolism and ATP production. CONCLUSIONS: EA could regulate mitochondrial dynamics to improve glucose metabolism dysfunction, thereby restoring motor function in MCAO.
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