NLRP3炎性小体活化可促进脑缺血再灌注损伤（CIRI）的进展。我们前期研究发现：降低4-羟基壬烯醛（HNE）水平，可抑制NLRP3炎性小体活化，减轻CIRI，但具体分子机制尚不清楚。考虑到HNE对蛋白的修饰（HNE修饰）会影响NF-κB的生物学效应；生物信息学分析显示NLRP3启动子区域存在NF-κB的结合位点。因此，我们推测HNE可能通过蛋白修饰激活NF-κB，导致NLRP3炎性小体活化，促进CIRI的进展。为验证该假说，本研究将在体/外进一步明确HNE对NLRP3炎性小体活化的调控作用及对CIRI的影响；利用RNA干扰等方法探讨NF-κB信号通路及其HNE修饰、修饰部位的点突变以及HNE清除剂对此过程的作用；利用ChIP等方法确定NF-κB对NLRP3基因的启动作用及关键结合位点。本课题的实施将进一步阐明HNE在CIRI的关键作用，为临床脑保护的药物靶点提供理论依据。

NLRP3 inflammasome activation can promote the progress of cerebral ischemia-reperfusion injury (CIRI). We previously found that decreasing HNE levels can inhibit the activation of NLRP3 inflammasome and reduces CIRI，but the mechanism is unclear; Considering that HNE modification of proteins (HNE modification) affects the biological effects of NF-κB; and bioinformatics prediction indicates that there is a NF-κB binding site in the NLRP3 promoter region. Therefore, we speculate that HNE may activate NLRP3 inflammasome through protein modification to activate NF-κB and promote the progress of CIRI. To test this hypothesis, this study seeks to clarify the effect of HNE on regulating the activation of NLRP3 inflammasome and the effect on CIRI in vitro and in vivo; using RNA interference and other methods to explore the NF-κB signaling pathway and its HNE modifications, point mutations at modified sites and the effects of HNE scavengers on this process; ChIP and other methods were used to confirm the initiation and key binding sites of NF-κB on NLRP3 gene. The implementation of this topic will further clarify the key role of HNE in CIRI, and provide a theoretical basis for clinical brain protection drug targets.