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Electroacupuncture promotes neural function recovery by alleviating mitochondria damage in cerebral ischemia mice
Feng Yashuo1, Guan Chong1, Yang Zhe2
1School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai 201203 China; Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, Shanghai 200040 China; National Center for Neurological Disorders, Shanghai 200040 China; National Clinical Research Center for Geriatric Diseases, Shanghai 200040 China.
Aims:
This study aimed to observe the effect of electroacupuncture (EA) at Zusanli point (ST36) on motor function of cerebral ischemia mice, and to observe the effect of EA on mitochondrial morphology of peri-infarct cortex neurons in cerebral ischemia mice.
Methods:
Middle cerebral artery occlusion (MCAO) was used to develop an ischemic stroke mice model. EA treatment was performed for three consecutive days for 15 min per day after MCAO modeling. We investigated the therapeutic effects of EA on MCAO mice by performing neurobehavioral assessment (modified Neurological Severity Score, Rotarod test, Open-field test and Gait analysis) and TTC staining. The morphology and function of neuronal mitochondria were evaluated by transmission electron microscopy, qRT-PCR, chemiluminescence, and western blot. Nissl staining, TUNEL staining and immunofluorescence staining were used to observe neuronal morphology and apoptosis. Furthermore, ELISA was employed to measure the expression levels of inflammatory factors in mouse serum.
Results:
EA alleviated motor dysfunction and infarct volume in mice with cerebral ischemia. It improved the neuronal mitochondria damage in MCAO mice, and decreased the protein and mRNA expression level of mitochondrial fission related proteins (FIS1 and Drp1). In addition, EA can reduce neuronal damage and apoptosis of nerve cells, and decrease the level of inflammatory factors (IL-1β, TNF-α, IL-6 and IL-8) in cerebral ischemia mice.
Conclusion:
EA therapy can improve motor dysfunction and alleviate the damage of neuron mitochondria in cerebral ischemic mice.
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