神经病理性疼痛发生机制的研究进展  

Research Advances in Mechanisms of Neuropathic Pain

作　　者：傅青雯 尤浩军[1] 雷静 FU Qingwen;YOU Haojun;LEI Jing(Translational Medicine Research Center for Sensory and Motor Diseases,Yan’an University,Yan’an 716000,Shaanxi,China)

机构地区：[1]延安大学感觉与运动疾病转化医学研究中心,中国陕西延安716000

出　　处：《生命科学研究》2023年第2期139-146,共8页Life Science Research

基　　金：国家自然科学基金资助项目(82074564,81860410,81772451)。

摘　　要：神经病理性疼痛(neuropathic pain,NP)作为一种常见、难治的慢性疼痛,由躯体感觉系统的损伤或疾病引起,临床表现以自发痛和诱发痛为主,给患者带来极大困扰。神经病理性疼痛相关机制尚未完全阐明,目前被广泛接受的神经病理性疼痛产生和维持的机制主要是神经损伤引起外周敏化和中枢敏化。引起外周敏化的因素包括交感神经芽生引起相关离子通道改变的异位放电活动、外周炎性反应、非编码RNA相关基因转录失调及疼痛信号传导变化等;诱发中枢敏化的因素除了相应炎症反应外,还包括神经胶质细胞异常活化以及中枢神经系统功能变化。本文就神经损伤引起外周敏化和中枢敏化的因素作相应综述,以期为神经病理性疼痛的基础研究及治疗提供新思路。Neuropathic pain(NP),as a common and refractory chronic pain,is caused by damage or diseases of the somatosensory system.The clinical manifestations are mainly spontaneous pain and induced pain,which bring great distress to patients.The mechanisms involved in NP have not been fully elucidated,and it has been widely accepted that peripheral and central sensitization after a nerve injury play critical roles in induction and maintenance of NP.Peripheral sensitization is mainly related to ectopic discharge induced by sympathetic sprouting associated with changes in related ion channels,peripheral inflammatory responses,transcriptional disorders of genes related to non-coding RNAs,and changes in pain signal transduction,while central sensitization is closely related to inflammatory responses,abnormal activation of glial cells and dysfunction of central nervous system.Herein,the mechanisms underlying peripheral and central sensitization resulted from nerve injuries were reviewed,hoping to provide new ideas for basic research on NP and its treatment.

关 键 词：神经病理性疼痛(NP) 外周敏化 中枢敏化 

分 类 号：Q421[生物学—神经生物学] R741[生物学—生理学]