NLRP3炎症小体在颅脑损伤中的研究进展

Advances in Research of NLRP3 Inflammasome in Traumatic Brain Injury

颅脑损伤可造成短暂性或永久性的中枢神经系统损伤,致死率和致残率均较高。神经炎症反应是中枢神经系统固有免疫系统的免疫应答机制,原发性和继发性损伤均可激活神经炎症反应,其中核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体在中枢系统炎症反应中起关键作用。颅脑损伤后,NLRP3炎症小体可通过经典和非经典途径激活,其各组分在颅脑损伤患者脑脊液中表达增加,并在颅脑损伤模型的损伤皮质中高表达。通过抑制NLRP3炎症小体激活下游炎症因子可以改善颅脑损伤的预后,减轻神经功能障碍。

Traumatic brain injury( TBI) causes transient or permanent damage to the central nervous system with high mortality and disability,The neuroinflammatory response is an immune response to the innate immune system in the central nervous system,and a series of primary and secondary injuries activate neuroinflammatory responses,where the nucleotidebinding oligomerization domain like receptor-3( NLRP3) inflammasome plays a key role in the CNS inflammatory response.After the brain is injured,the NLRP3 inflammasome is activated by canonical and non-canonical pathways. The expression levels of components of NLRP3 inflammasome are increased in cerebrospinal fluid of the TBI patients. In TBI model,it was also found to be increased in pericontusional cortex. By inhibiting NLRP3 inflammasome activation and downstream inflammatory factors,the prognosis of injury can be improved and neurological dysfunction can be alleviated. This review focuses on the mechanism of NLRP3 inflammasome activation and regulation,and further explores the role of NLRP3 inflammasome in injury.