小胶质细胞NLRP3炎性小体在PND中的研究进展

Research on the NLRP3 Inflammasome in Microglia in PND Progress

摘要: 围术期神经认知障碍(perioperative neurocognitive disorder, PND)是手术后尤其是老年患者术后常见的神经系统并发症，其病理机制错综复杂，近年来，主流观点认为神经炎症是PND发病的核心环节之一。小胶质细胞作为中枢神经系统重要的免疫细胞在其中有不可或缺的作用。研究表明，NOD样受体热蛋白结构域相关蛋白3 (NOD-like receptor family pyrin domain-containing 3, NLRP3)炎症小体作为先天免疫系统中重要的胞内免疫传感器，广泛表达于小胶质细胞中。研究表明，NLRP3炎症小体可通过调控小胶质细胞的极化、焦亡及自噬等生理病理过程，深度参与PND的发生发展。炎症小体可通过调控小胶质细胞的极化、焦亡及自噬等生理病理过程，深度参与PND的发生发展。本文结合最新研究进展，围绕小胶质细胞中NLRP3炎性小体参与PND的病理过程，及其在小胶质细胞M1型极化、焦亡及自噬中的作用机制，并探讨了相关治疗方案，为后续研究提供方向。

Abstract: Perioperative neurocognitive disorder (PND) is a common neurological complication following surgery, particularly in elderly patients. Its pathophysiological mechanisms are complex; in recent years, the prevailing view has been that neuroinflammation is one of the key factors in the pathogenesis of PND. Microglia, as important immune cells in the central nervous system, play an indispensable role in this process. Research indicates that the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, as a key intracellular immune sensor within the innate immune system, is widely expressed in microglia. Studies have shown that the NLRP3 inflammasome is deeply involved in the onset and progression of PND by regulating physiological and pathological processes in microglia, such as polarisation, pyroptosis and autophagy. The inflammasome plays a pivotal role in the pathogenesis and progression of PND by regulating physiological and pathological processes in microglia, such as polarisation, pyroptosis and autophagy. This article reviews the latest research findings, focusing on the role of the NLRP3 inflammasome in the pathological processes of PND within microglia, as well as its mechanisms of action in M1-type polarisation, pyroptosis and autophagy. It also explores relevant therapeutic strategies, thereby providing a direction for future research.