七氟烷临床应用导致的术后认知功能障碍（POCD）是麻醉领域的难题之一，小胶质细胞介导的神经炎症在POCD中的作用日益突显。申请人在前一项NSFC资助下观察到七氟烷诱导的POCD大鼠海马IL-1β等炎症因子的表达增强，而IL-1β主要由NLRP3炎症小体介导成熟和分泌。已知小胶质细胞NLRP3炎症小体活化参与抑郁和阿尔兹海默症等神经损伤，但其在七氟烷诱导的POCD中的作用尚未明确。申请人推测七氟烷活化小胶质细胞NLRP3炎症小体，诱导海马区神经炎症，可能是七氟烷诱发POCD的新机制。本项目拟从动物、细胞和分子水平探讨①NLRP3炎症小体在七氟烷诱导大鼠POCD中的作用；②七氟烷活化小胶质细胞NLRP3炎症小体的分子机制；③七氟烷对小胶质细胞自噬的影响及其与NLRP3炎症小体活化和POCD的关系。最终进一步揭示七氟烷诱导大鼠POCD的分子机制，为减轻七氟烷导致的神经功能损伤提供有力的实验依据。

Postoperative cognitive dysfunction (POCD) caused by the clinical application of sevoflurane is one of the problems in the field of anesthesia. The role of microglial mediated neuroinflammation in POCD is increasingly prominent. In the previous study of NSFC, we observed increased expression of inflammatory cytokines such as IL-1β in the hippocampus of POCD rats induced by sevoflurane, while.IL-1β is mainly mediated by NLRP3 inflammasome. It is known that NLRP3 inflammasome of microglial cells is involved in the nerve injury such as depression and alzheimer's, but its role in the POCD induced by sevoflurane is not clear. It is speculated that sevoflurane activates NLRP3 inflammasome and induces neuroinflammation in the hippocampus, which may be a new mechanism of sevoflurane-induced POCD. The purpose of this project is to explore the role of NLRP3 inflammasome in POCD in rats induced by sevoflurane in rats, cells and molecular levels. The molecular mechanism of NLRP3 inflammasome in the activated microglia cells; Effects of sevoflurane on autophagy of microglia and its relationship with NLRP3 inflammasome activation and POCD. Together, the molecular mechanism of sevoflurane induced POCD in rats was further revealed to provide a powerful experimental basis for reducing the neurological impairment caused by sevoflurane.