神经病理性疼痛是由神经系统原发性损害和功能障碍所激发或引起的疼痛，炎症作为神经病理性疼痛发展的重要病机之一，是生物体对组织损伤做出的一种正常生理反应。炎症介导的神经病理性疼痛发展机制与外周神经敏化、中枢神经敏化息息相关，包括神经炎症反应、氧化应激反应、离子通道改变、胶质细胞的活化。常见的中药成分马钱子碱、小檗碱、去氢紫堇鳞茎碱、川芎嗪、氧化苦参碱、青藤碱均可缓解神经病理性疼痛。生物碱可通过多条途径影响神经病理性疼痛，其发挥的抗炎作用影响着外周神经敏化和中枢神经敏化，是治疗神经病理性疼痛的重要机制之一。因此生物碱介导的炎症反应具有良好的抗神经元损伤作用，对神经病理性疼痛产生一定的治疗作用。总结了炎症参与神经病理性疼痛和生物碱抗炎镇痛的机制，拟从分子层面阐释生物碱发挥抗神经病理性疼痛的作用机制。

Neuropathic pain is motivated and caused by primary damage and dysfunction of the nervous system. As one of the important pathogenesis of neuropathic pain, inflammation is a normal physiological response of organisms to tissue damage. The mechanism of inflammation-mediated neuropathic pain development is closely related to peripheral nerve sensitization and central nerve sensitization, including neuroinflammation, oxidative stress, changes in ion channels, and activation of glial cells. The common traditional Chinese medicine active components, such as strychnine, berberine, dehydrovioletine, ligustrazine, oxymatrine, and sinomenine can relieve neuropathic pain. Alkaloids can affect neuropathic pain through multiple pathways, and their anti- inflammatory effects affect peripheral nerve sensitization and central nerve sensitization, and it is one of the important mechanisms for the treatment of neuropathic pain. Therefore, alkaloid-mediated inflammatory response has good anti-neuron damage and has a certain therapeutic effect on neuropathic pain. This paper summarizes the mechanism of inflammation involved in neuropathic pain and alkaloids anti-inflammatory and analgesic, and intends to elucidate the mechanism of alkaloids exerting anti-neuropathic pain at the molecular level.

R971

贵州中医药大学第二附属医院院内科研项目(GZEYK[2020]13号)