蛛网膜下腔出血（SAH）后神经损伤、修复与其临床预后密切相关，但目前对其具体机制认识甚微。我们前期研究发现在炎性反应逐渐消退、神经修复逐渐主导的SAH后期，小胶质细胞作为神经炎性反应的核心，并未回归至静息态，反而呈现出长时程激活状态；且SAH早期以M1型为主，后期则以M2型为主。结合国际研究及前期工作，课题组推测Sall1作为小胶质细胞特异性表达的核心调控分子，可能参与调控SAH后小胶质细胞由M1型向M2型转化，从而加速神经修复。本课题拟构建体内、体外SAH模型，从神经损伤和神经修复两方面出发，立足于小胶质细胞的表型功能转化，运用RNA干扰与基因过表达技术，全面探讨Sall1调控的小胶质细胞表型功能转化在SAH后神经损伤与修复中的具体作用机制。通过此项研究，将有助于深入理解SAH后神经损伤与修复的内源性调控机制，为SAH早期临床干预提供新的治疗靶点，并奠定理论基础。

The prognosis of subarachnoid hemorrhage (SAH) is closely related to neural injury and neural repair, however, little is known about its specific mechanisms. Our previous studies found that microglia, as the key factor of inflammatory response, did not return to the resting state but showed a long-term activation state in the late stage of SAH. However, in this stage, the inflammatory response gradually subsided and neural repair gradually dominated. In addition, the M1 type was predominant in the early stage while the M2 type was predominant in the late stage of SAH. Based on international research and previous work, we speculated that Sall1, as a key specific regulatory factor of microglia, might be involved in the regulation of microglial transformation from M1 to M2 after SAH, thus accelerating neural repair. In this study, we are planning to apply RNA interference and gene overexpression aiming at Sall1 to investigate the mechanisms of Sall1 in neural injury and repair following SAH, which will be validated through phenotypic functional transformation of microglia both in vivo and in vitro. From this research, we expect to better understand the specific pattern and mechanisms of neural injury and repair after SAH, thereby providing a novel therapeutic target and laying a theoretical foundation for SAH.