血脑屏障（BBB）破坏是脓毒症脑病（SAE）发生发展的主要原因，但机制不明。我们前期采用高通量基因测序发现，Maf1在受炎症损伤的BBB内皮细胞中表达增加；进一步在LPS诱导的BBB炎症模型中发现，过表达Maf1可抑制内皮细胞凋亡。提示Maf1可能对脓毒症BBB损伤起着重要的保护作用，而目前尚无Maf1与脓毒症脑病时BBB之间关系的报道。另外，我们还发现Maf1在抑制内皮细胞凋亡的过程中，炎症因子表达下调，但现有的研究也未发现Maf1可抑制炎症。故：Maf1是否可抑制炎症通路来保护性地调控BBB，从而发挥防治脓毒症脑病的效应？本研究拟构建SAE和BBB炎症损伤模型分别进行体内、体外实验，利用AAV过表达和沉默Maf1基因，以评价Maf1对脓毒症脑病的作用，并深入研究Maf1在BBB损伤中对炎症通路的影响及作用位点，旨在阐明Maf1调控SAE的核心机制，为SAE治疗提供新的理论依据。

The damage of the blood-brain barrier (BBB) is the leading cause of sepsis-associated encephalopathy (SAE), but the mechanism is unclear. In previous study, we found that the expression of Maf1 in BBB endothelial cells was increased via gene sequencing. Further, overexpression of Maf1 could inhibit endothelial cell apoptosis induced by LPS, suggesting that Maf1 may play an important protective role in sepsis-induced BBB injury. However, there is no report on the relationship between BBB and Maf1 in SAE. In addition, we also found that Maf1 inhibited endothelial cell apoptosis accomplishing with inflammatory factor expression down-regulation. Whether Maf1 could protect BBB via inflammatory pathway to inhibit the development of SAE? Therefore, in the present study, we construct the model of SAE and model of blood-brain barrier inflammatory injury to evaluate the effect of Maf1 on inflammatory pathways as well as possible targets for BBB injury via adenovirus associated virus vector, aiming to elucidate the core mechanism of Maf1 in regulating SAE and find a new target for the treatment of SAE.