神经肌电刺激通过调控炎症因子促进小鼠脊髓损伤修复研究

doi:10.13418/j.issn.1001-165x.2023.4.08

Abstract

Abstract: Objective To investigate the mechanism of neuromuscular electrical stimulation (NMES) regulating the expression of inflammatory factors in repairing spinal cord injury (SCI). Methods Sixty healthy adult mice were randomly divided into a Sham group, a SCI group, a 1 Hz NMES group, a 20 Hz NMES group, 15 mice in each group. Basso Mouse Scale (BMS) score and footprint analysis were used to observe the recovery of hindlimb motor function of mice. Immunofluorescence was used to observe the number of anterior horn neurons of spinal cord injury. Real-time RT-PCR was used to detect the expression of inflammatory factors TNF-α, IL-6 and IL-12 mRNA. Western Blot was used to determine the inflammatory factors TNF-α, IL-6, IL-12 and the expression of BDNF, GFAP. Results Compared with the SCI group, the hindlimb motor function of mice was significantly improved after the neuromuscular electrical stimulation intervention, and the number of surviving neurons at the injury site was increased, and the number of neurons in the 20 Hz NMES group was more than that in the 1 Hz NMES group. Neuromuscular electrical stimulation intervention could down-regulate the expression of TNF-α, IL-6, IL-12 and GFAP, and promote the expression of BDNF. Conclusions Neuromuscular electrical stimulation can down-regulate inflammatory factors, inhibit the expression of GFAP, inhibit glial scarring, and up-regulate the expression of BDNF to protect the number of neurons, and promote the recovery of motor function in mice after spinal cord injury.

Key words: Spinal cord injury, , , , Neuromuscular electrical stimulation, , , Inflammatory factor, Functional recovery

CLC Number:

Liang Yinhua, Song Haiwang, Jiang Guanhua, Lou Yi, Liu Guoxiang, Yang Dan . Neuromuscular electrical stimulation accelerates spinal cord injury repair by regulating inflammatory factors [J]. Chinese Journal of Clinical Anatomy, 2023, 41(4): 416-421.

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Neuromuscular electrical stimulation accelerates spinal cord injury repair by regulating inflammatory factors

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