蛛网膜下腔出血(SAH)致死率及致残率高，其所致脑损伤目前无有效药物。本团队研究发现，高迁移率族蛋白B1（HMGB1）在SAH后早期促进炎症反应，加重脑损伤。但在SAH后期，HMGB1仍然处于高表达状态，但此时脑水肿及脑损伤并不加重。HMGB1在SAH后期的作用及机制仍然是空白。我们假设HMGB1在SAH后存在双相的作用机制，在SAH早期，HMGB1主要为还原型，通过TLR4受体发挥促炎作用，在SAH晚期，HMGB1转变为氧化型，并通过RAGE受体，促进神经营养因子的分泌，促进卒中后神经血管的重塑。为了验证这一假说，我们采用大鼠SAH模型，采用western blot、免疫组化、免疫荧光、串联质谱分析、流式细胞仪等手段，从分子、细胞、组织以及动物整体水平等多方面探讨HMGB1在SAH后期中的作用，并明确其机制，为SAH后脑损伤的修复机制提供新的认识。

SAH especially, aneurismal SAH (aSAH) was a life-threatening disease. High-mobility group box 1(HMGB1), as a nonhistone protein binding with DNA, is widely expressed in the nucleus of nearly all eukaryotic cells, including the brain cells, and stabilizes nuclesome formation, facilitates gene transcription. Our previous study indicated that HMGB1 was released early from neurons after SAH onset and played a vital role in triggering inflammation after SAH. Our preliminary work also suggested that HMGB1 remained at a high level in the late stage of SAH. However, the brain water content in the late stage of SAH was as normal as sham group which indicated the inflammation or brain injury was not serious. Little was known about effect of HMGB1 in the late stage of SAH. Previous studies also indicated that HMGB1 could induce many neurotrophic factors, such as nerve growth factor, basic fibroblast growth factor, platelet-derived growth factor, brain-derived neurotrophic factor, ciliary neurotrophic factor, neuropilin-1, vascular endothelial growth factor and others. Thus we hypotheses that HMGB1 played a benefit role in the late stage of SAH. We will use rat SAH models, with the help of western blot, real-time polymerase chain reaction, immunofluorescence, tandem mass spectrometric analysis method and flow cytometry to understand the role and detailed mechanism of HMGB1 played in the late stage of SAH.