Yang Pu, Chen Hai-Yan, Zhang Xi, Wang Tian, Li Ling, Su Hong, Li Jing, Guo Yan-Jun, Su Sheng-Yong
Guangxi University of Chinese Medicine, Nanning, Guangxi, People's Republic of China.
The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning, Guangxi, People's Republic of China.
J Pain Res. 2023 Jul 18;16:2447-2460. doi: 10.2147/JPR.S415111. eCollection 2023.
Cervical spondylotic radiculopathy (CSR) is a common neurologic condition that causes chronic neck pain and motor functions, with neuropathic pain (NP) being the primary symptom. Although it has been established that electroacupuncture (EA) can yield an analgesic effect in clinics and synaptic plasticity plays a critical role in the development and maintenance of NP, the underlying mechanisms have not been fully elucidated. In this study, we explored the potential mechanisms underlying EA's effect on synaptic plasticity in CSR rat models.
The CSR rat model was established by spinal cord compression (SCC). Electroacupuncture stimulation was applied to LI4 () and LR3 () acupoints for 20 min once a day for 7 days. Pressure pain threshold (PPT) and mechanical pain threshold (MPT) were utilized to detect the pain response of rats. A gait score was used to evaluate the motor function of rats. Enzyme-linked immunosorbent assay (ELISA), Western blot (WB), immunohistochemistry (IHC), immunofluorescence (IF), and transmission electron microscopy (TEM) were performed to investigate the effects of EA.
Our results showed that EA alleviated SCC-induced spontaneous pain and gait disturbance. ELISA showed that EA could decrease the concentration of pain mediators in the cervical nerve root. WB, IHC, and IF results showed that EA could downregulate the expression of synaptic proteins in spinal cord tissues and promote synaptic plasticity. TEM revealed that the EA could reverse the synaptic ultrastructural changes induced by CSR.
Our findings reveal that EA can inhibit SCC-induced NP by modulating the synaptic plasticity in the spinal cord and provide the foothold for the clinical treatment of CSR with EA.
神经根型颈椎病(CSR)是一种常见的神经系统疾病,可导致慢性颈部疼痛和运动功能障碍,神经性疼痛(NP)是其主要症状。尽管电针(EA)在临床上已被证实具有镇痛作用,且突触可塑性在NP的发生和维持中起关键作用,但其潜在机制尚未完全阐明。在本研究中,我们探讨了电针在CSR大鼠模型中对突触可塑性影响的潜在机制。
通过脊髓压迫(SCC)建立CSR大鼠模型。每天一次对大鼠的足三里穴(LI4)和太冲穴(LR3)进行20分钟的电针刺激,持续7天。采用压力疼痛阈值(PPT)和机械疼痛阈值(MPT)检测大鼠的疼痛反应。用步态评分评估大鼠的运动功能。采用酶联免疫吸附测定(ELISA)、蛋白质免疫印迹法(WB)、免疫组织化学(IHC)、免疫荧光(IF)和透射电子显微镜(TEM)研究电针的作用。
我们的结果表明,电针可减轻SCC诱导的自发疼痛和步态障碍。ELISA结果显示,电针可降低颈神经根中疼痛介质的浓度。WB、IHC和IF结果表明,电针可下调脊髓组织中突触蛋白的表达并促进突触可塑性。TEM显示,电针可逆转CSR诱导的突触超微结构变化。
我们的研究结果表明,电针可通过调节脊髓中的突触可塑性来抑制SCC诱导的NP,为电针临床治疗CSR提供了依据。