新生儿缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)是导致新生儿死亡和婴幼儿伤残的主要原因,发病机制包括细胞能量代谢衰竭、血管源性脑水肿、兴奋性氨基酸神经毒性、氧化应激、炎症反应等的交互作用,其中炎症反应是重要的病理生理过程,涉及NLRP3(NOD-like receptor thermal protein domain associated protein 3)/caspase-1/IL-1β信号通路的激活,促进白细胞介素-1β(inter-leukin-1β,IL-1β)等炎症因子成熟与释放,诱导神经细胞焦亡.本文就NLRP3/caspase-1/IL-1β信号通路的概述、激活途径、介导HIBD的作用机制及HIBD治疗的相关新进展等方面进行综述,以期为HIBD的神经保护策略提供新思路.
Roles of NLRP3 inflammasome/caspase-1/IL-1β signaling pathway in hypoxic-ischemic brain damage
Neonatal hypoxic-ischemic brain damage(HIBD)is the main cause of neonatal death and infant disability.The pathogenesis includes the interaction of cell energy metabolism failure,vasogenic brain edema,excitatory amino acid neurotoxicity,oxidative stress and inflammation,among which inflammation is an important pathophysiological process.It involves the activation of NLRP3/caspase-1/IL-1β signaling pathway,promotes the maturation and release of interleukin-1β(IL-1β)and other inflammatory factors,and induces pyroptosis of nerve cells.This article reviews the structure,activation pathway of NLRP3/caspase-1/IL-1β signaling pathway,the mechanism mediating HIBD and the recent progress in HIBD treatment,so as to provide new ideas for the neuroprotective strategies of HIBD.
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