蛛网膜下腔出血(SAH)后早期发生的神经元凋亡是影响患者神经功能预后的重要病理过程。巨噬细胞集落刺激因子(CSF-1)可作用于其特异性受体CSF-1R调控单核/巨噬细胞增值、生长、分化，但其对神经元的作用尚未阐明。我们前期研究发现，SAH术后的小鼠皮层神经元大量表达CSF-1R。SAH术后予以实验小鼠rCSF-1可以显著改善其短期神经功能，减少大脑皮层神经元凋亡，并显著上调PI3K及PDK1磷酸化水平。由于目前未见关于神经元CSF-1R在急性脑血管病中相关作用的报道。我们基于前期研究基础提出以下假说：CSF-1R在SAH后早期可通过激活PI3K/PDK1信号通路，抑制神经元凋亡，发挥神经保护作用。本项目拟从分子、细胞和动物水平出发，明确CSF-1R激活对SAH后早期神经元凋亡的影响，探讨CSF-1R通过调控PI3K/PDK1通路影响神经元凋亡的机制，希望为改善SAH患者功能预后提供新靶点。

Neuronal apoptosis is considered a crucial therapeutic target for interventions against early brain injury (EBI) after subarachnoid hemorrhage (SAH). Colony stimulating factor 1 (CSF-1) is a well-known regulator in the survival, proliferation, and differentiation of mononuclear phagocytes by stimulating CSF-1R, its specific receptor. However, the effects of CSF-1/CSF-1R in neurons remain unclear. Our previous study observed significantly upregulated express of CSF-1R in neurons of cortex after SAH in mouse. Further investigation indicated that exogenous recombinant CSF-1 could attenuate neuronal apoptosis, reserve short-term neurological function, and promote phosphorylation of PI3K and PDK1 after SAH. Since the role of CSF-1R has not been reported though our literature review, we proposed a hypothesis that activation of CSF-1R could attenuate neuronal apoptosis and reserve neurological function via PI3K/PDK1 signaling pathway in EBI after SAH. This study aims to verify the neuroprotective role of CSF-1R activation against neuronal apoptosis and understand the potential mechanism underlying by investigating the effects of CSF-1R mediated PI3K/PDK1 signaling pathway after SAH. We hope this study could provide sufficient evidences on levels of animal subjects, tissues, cells, and molecules to understand the role of CSF-1R as a potential therapeutic target in SAH.