蛛网膜下腔出血（SAH）后神经修复是影响患者预后的重要因素，但其具体机制仍不明确。我们研究发现：SAH后颞叶皮层负向调控炎性反应的CD24表达增高，同时发现除胶质细胞外，神经元中CD24也明显上调。我们推测CD24在SAH后可能不只是参与调控炎性反应，同时具有其他重要功能。对此，我们预实验发现SAH后神经发生区域（海马齿状回和室管膜下区）内CD24同样被上调，且表达时相明显早于颞叶皮层。结合国际相关研究，我们提出假说：SAH后脑内神经发生区域中的神经干细胞发生增殖、分化和迁移，而CD24作为其潜在标志物可在脑内各区域全面上调，最终在神经修复中发挥重要作用。本课题拟通过体内、体外实验，针对CD24运用RNA干扰及基因过表达技术，立足神经再生模式，探讨CD24在SAH后神经修复中的作用机制。通过此项研究，将有助于深入理解SAH后神经修复的具体模式与机制，为SAH临床治疗与康复提供新的靶点。

Neuronal repair is a key regulator of prognosis in patients with subarachnoid hemorrhage (SAH), however, the specific mechanisms have not been well elucidated. We previously found that cortical CD24 could be elevated following SAH. Meanwhile, we occasionally found that CD24 was upregulated not only in glial cells but also in neurons. Accordingly, we speculated that CD24 might play an important role in some others fields as well as in inflammatory response. Therefore, we performed our pre-experiments and found that CD24 was upregulated much earlier in neurogenesis areas (hippocampal dentate gyrus and subventricular zone) than that in temporal cortex. Based on the related research in the world, we raised a hypothesis that the neurogenesis could be activated after SAH, and neural stem cells had an increased proliferation, differentiation and immigration. CD24, as a marker of these cells, could be elevated in the brain, thus contributing to the neuronal repair following SAH. In this study, we are planning to apply RNA interference and gene overexpression aiming at CD24 to investigate the mechanisms of CD24 in neuronal repair following SAH, which will be validated through neuronal regenerative pattern both in vivo and in vitro. From this research, we expect to better understand the specific pattern and mechanisms of neuronal repair after SAH, thereby providing a novel therapeutic target for SAH.