脊髓胶质细胞在神经病理性痛作用机制的研究进展
Modulation Effect of Spinal Glial Cells in Neuropathic Pain
本研究旨在探讨脊髓胶质细胞调控神经病理性痛的具体机制。近年来研究发现在神经病理性疼痛中脊髓小胶质细胞和星形胶质细胞被激活,TLR4、IL-1β、nNOS、MMP2、MMP9等细胞因子及Fractalkine等趋化因子增加, ERK1/2 等信号通路被激活,此外,研究表明激活的小胶质细胞参与早期神经病理性痛阶段疼痛的形成,星形胶质细胞参与调制神经病理性疼痛维持。而抑制脊髓胶质细胞的活性会使炎性因子的表达量下降,表明胶质细胞参与机体病理性痛调制过程,其机制通过抑制脊髓胶质细胞活性,抑制神经元-神经胶质细胞通路的活性,从而抑制神经元兴奋性;受抑制的胶质细胞不会释放炎性因子、神经递质、细胞营养因子等物质,同时又抑制ERK1/2 信号通路,抑制痛觉信息的转导进而缓解神经病理性痛。
his study was aim to investigate the mechanisms underlying the modulation effect of spinal glial cells in neuropathic pain. In recent years, the studies showing that spinal cord microglia and astrocytes are activated in neuropathic pain .Then the TLR4, IL-1β, nNOS, MMP2, MMP9, CGRP, and fractalkine are increased, and the ERK1/2 signaling pathways are activated in neuropathic pain. In addition, the studies have shown that activated microglia are involved in the formation of pain during early stages of neuropathic pain and that astrocytes are involved in the modulation of neuropathic pain maintenance. Inhibition of spinal glial activity will decrease the expression of inflammatory cytokines, indicating that glial cells involved in the pathogenesis of pathological pain. Its mechanism inhibits neuronal excitability by inhibiting glial cell and neuronal - glial cell viability.The inhibition of glial activation which will not release inflammatory cytokines, neurotransmitters, cell nutrition factors and other substances, while inhibiting the ERK1 / 2 signaling pathway, inhibit the transduction of pain information and thus alleviate neuropathic pain.
卢秋华、阮丽钦、杨佳佳、程林洁、王冬梅、晏燕花
神经病学、精神病学基础医学生物科学理论、生物科学方法
胶质细胞神经病理性痛炎性因子信号通路
glial cellneuropathic paininflammatory cytokinessignaling pathway
卢秋华,阮丽钦,杨佳佳,程林洁,王冬梅,晏燕花.脊髓胶质细胞在神经病理性痛作用机制的研究进展[EB/OL].(2018-02-13)[2025-08-16].http://www.paper.edu.cn/releasepaper/content/201802-79.点此复制
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