缺血性脑卒中正严重威胁人类生命健康，促进脑损伤后神经功能的修复是亟待解决的医学难题。我们前期研究发现七氟烷可通过激活小胶质细胞促进SVZ区神经干细胞的增殖和分化，加速神经功能的修复重建，但七氟烷调控小胶质细胞发挥促进内源性神经再生的分子机制尚待研究。预实验结果显示七氟烷可上调小胶质细胞上TREM2/DAP12复合体的表达，而文献报道TREM2/DAP12是小胶质细胞活化的调节器。因此，我们推测：七氟烷可通过调控TREM2/DAP12选择性活化小胶质细胞，促进小胶质细胞的吞噬功能和抗炎反应，通过Wnt/β-catenin信号通路促进内源性神经再生。本课题拟利用形态学、细胞分子生物学、电生理、行为学和小动物MRI等技术，研究七氟烷通过选择性活化小胶质细胞促进神经再生和修复重建的分子机制，给缺血性脑卒中的修复重建治疗提供新思路，为七氟烷用于缺血性脑卒中防治的转化研究提供坚实的实验依据。

Ischemic stroke is a major health problem and social burden around the world with almost no cure. Accelerating neurogenesis and repair after brain ischemic injury is increasingly important. Previously, we found that sevoflurane could activate more microglia earlier, and accelerate the neuroblast proliferation in the SVZ and the neuroblast migration to the infarct to differentiation. However, the molecular and cellular mechanisms underlying that sevoflurane activates microglia and promoting neurogenesis are still unclear. Our unpublished data showed that sevoflurane could induce the upregulation of TREM2/ DAP12 in microglia. Recent works report that TREM2/DAP12 complex is the modulator for the microglia activation. Thus, we hypothesize that sevoflurane could selectively induce the activation of microglia by acting on TREM2/DAP12 complex, and then promote endogenous neurogenesis via Wnt-β-catenin signaling pathway. In this study, by the morphological, molecular and cellular, electrophysiological, behavioral, and MRI tests, we plan to explore the molecular and cellular mechanisms underlying the activation of microglia by sevoflurane and to investigate that activated microglia could promote the process of endogenous neurogenesis following ischemic stroke. This study will provide a solid experimental and theoretical basis for the translational study of sevoflurane in the prevention and treatment for ischemic stroke