NLRP3、AIM2炎症小体在创伤性脑损伤中作用的研究进展

Research advances in role of NLRP3 and AIM2 inflammasome in traumatic brain injury

创伤性脑损伤(traumatic brain injury,TBI)是一个全球重要公共卫生问题,具有高发生率、高致残率和高死亡率。炎症小体是一种多聚蛋白复合物,它可以识别细胞损伤或病原微生物感染的信号,通过经典和非经典途径激活,促使白细胞介素(interleukin,IL)-1β和IL-18的成熟和分泌,从而引起炎症反应。近年来,随着相关研究的不断深入,炎症小体在TBI中的重要作用被不断发现。本文对炎症小体在TBI中的作用进行综述,归纳总结NLRP3、AIM2炎症小体参与炎症反应的相关调节机制及其与TBI之间的关系,以期为今后该领域的研究提供参考。

Traumatic brain injury(TBI)is an important global public safety problem with high morbidity,disability and mortality.Inflammasome is a polymeric protein complex that recognizes signals of cell damage or pathogenic microbial infection,which can be activated through classical and non-classical pathways,and it promotes the maturation and secretion of IL-1βand IL-18,leading to inflammatory response.In recent years,with the deepening research of inflammasome,the important role of inflammasome in TBI has been increasingly recognized.In this paper,the role of inflammasome in TBI is reviewed,and the regulatory mechanism of inflammasome involved in inflammatory response and its relationship with traumatic brain injury are summarized,in order to provide evidence for future studies in this field.