早期脑损伤（EBI）是蛛网膜下腔出血（SAH）病残率增高的主要原因，神经再生在脑损伤后发挥关键的内源性保护效应。新近研究提示CX3CR1调控的小胶质细胞活化后形态转换（M1→M2）与神经再生关系密切；我们研究发现大鼠SAH后小胶质细胞活化与海马神经元前体细胞（NPCs）增殖在时间上吻合，现已证实CD200/CD200R是该两细胞间相互作用的重要机制。据此我们提出“小胶质细胞形态转换参与海马NPCs增殖,促进SAH后神经再生”的假设。该项目拟通过大鼠SAH模型及神经干细胞+小胶质细胞共培养模型，分步探讨：①SAH后小胶质细胞活化的表型特点；②CX3CR1受体激活能否增加SAH后M2型小胶质细胞活化并促进海马NPCs增殖；③干预CD200/CD200R细胞间直接作用对SAH后神经再生的影响。本项目着眼临床常见病，紧扣神经再生热门领域，探讨细胞间直接作用，有望为SAH早期脑损伤提供新的防治策略。

Early Brain Injury (EBI) results in high disability rate following Subarachnoid hemorrhage (SAH) and neurogenesis is a critical endo-neuroprotective mechanism following central nervous pathological condition. It has been proved that CX3CR1-conducted microglial type-transformation was strongly related with hippocampal neurogenesis and our previous study demonstrated that microglial activation was timely consistent with the mobilization of hippocampal neuron precursor cells (NPCs). CD200/CD200R maybe critical molecular correlation between these cells as reported. Here, we hypothesized that the type-transformation of microglia enhanced the microglia-NPCs dialogue, which was involved in hippocampal neurogenesis following SAH. With SAH model of rat and microglia- NSCs (neural stem cells) co-culture, we aim to elucidate whether activation of CX3CR1 can transfer activated microglia to a protective type (M2) and maintain it following SAH. Based on this, we are going to study the mutual effects between microglia and NPCs and the underlined chemical mechanism as CD200/CD200R. The project focused on the neurogenesis after SAH firstly from the sight of the neuroprotective effect of micrglia, which may confer a new therapeutic strategy for early brain injury following SAH.