Department of Immunology, Medical College of Qingdao University, Qingdao, Shandong 266071, PR China.
School of Emergency Medicine, Medical College of Qingdao University, Qingdao, Shandong 266071, PR China.
Int Immunopharmacol. 2022 Sep;110:109026. doi: 10.1016/j.intimp.2022.109026. Epub 2022 Jul 22.
Nerve injury and nerve pain are common diseases caused by neuroinflammation. Numerous studies have shown that the activation of NLRP3 (nod-like receptor family, pyrin domain-containing 3) inflammasome is involved in a various inflammatory response, such as Alzheimer's disease, diabetes, nerve damage and other diseases. The NLRP3 inflammasome is a complex containing NLRP3 protein, ASC (apoptosis-associated speckle-like protein), and pro-caspase-1, which is highly expressed and activated to promote the secretion of IL-1β and IL-18 in response to the stimulation of danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) in immune cells such as macrophages and dendritic cells. The activation of NLRP3 inflammasome can cause cell death through caspase-1-mediated cell pyroptosis and plays an important role in the development of nervous system injury and inflammation-related diseases. This discussion aims to summarize the mechanisms of nerve damage and pain caused by excessive activation of the NLRP3 inflammasome.
神经损伤和神经痛是由神经炎症引起的常见疾病。大量研究表明，NLRP3（核苷酸结合寡聚化结构域样受体家族，pyrin 结构域包含 3）炎性小体的激活参与了各种炎症反应，如阿尔茨海默病、糖尿病、神经损伤等疾病。NLRP3 炎性小体是一种包含 NLRP3 蛋白、ASC（凋亡相关斑点样蛋白）和 pro-caspase-1 的复合物，在受到巨噬细胞和树突状细胞等免疫细胞中危险相关分子模式（DAMPs）和病原体相关分子模式（PAMPs）的刺激后，高度表达并激活，以促进 IL-1β 和 IL-18 的分泌。NLRP3 炎性小体的激活可通过 caspase-1 介导的细胞焦亡引起细胞死亡，并在神经系统损伤和炎症相关疾病的发展中发挥重要作用。本讨论旨在总结 NLRP3 炎性小体过度激活引起的神经损伤和疼痛的机制。
