脑出血(ICH)后神经功能缺损是影响其预后的重要难题，目前仍缺乏有效的治疗药物。内源性神经干细胞(EnNSCs)活化以神经发生为特征，是ICH的损伤修复方式和潜在治疗手段。然而，ICH后EnNSCs神经发生受限，难以迁移至血肿周围、替代损伤脑组织。因此，药物增强神经发生可能成为ICH治疗的新策略。Compound-K是项目申请人首次报道的肝X受体(LXR)激动剂，前期工作初步证实能促进EnNSCs神经发生，而既往研究表明LXR是神经发生启动的重要信号。因此，Compound-K可能通过激活LXR促进神经发生，改善ICH后神经功能缺损。本项目拟采用Nestin-GFPTg/+和LXR-/-小鼠，通过免疫荧光及荧光共振能量传递等方法，系统阐明Compound-K对动物神经发生及功能预后的影响及机制；该项目不仅为ICH的治疗提供新的药物靶点，也为活化EnNSCs的治疗策略奠定理论基础。

Neurologic impairment is one of the important problems which affect the prognosis of intracerebral hemorrhage(ICH), there is still lack of effective treatments. Endogenous neural stem cells (EnNSCs) activation is characterized by neurogenesis, which is the repair method and potential treatment of ICH injury. However, Neurogenesis of EnNSCs is limited and difficult to migrate to hematoma for replacing the damaged brain tissue after ICH. Enhancing neurogenesis by drugs may be a new strategy for treating ICH. We reported for the first time that compound-K is a new LXR agonist, which has been preliminarily confirmed to promote EnNSCs neurogenesis. Also previous studies show that LXR is an important signal of neurogenesis. Therefore, Compound-K may promote neurogenesis and improve neurologic deficits by activating LXR after ICH. In this proposal, we will study the effects of Compound-K on neurogenesis and functional outcomes by using immunofluorescence and Fluorescence resonance energy transfer technology, and testing in Nestin-GFPTg/+ and LXR knockout mice. Our project not only provide a new target for the treatment of ICH, but also lay theoretical foundation for the treatment strategy of activating EnNSCs.