低氧诱导因子-1α（hypoxia-inducible factor-1α, HIF-1α）是低氧反应的主要调节因子。大量研究表明脑缺氧时，HIF-1α表达增加，可激活糖酵解、血管生长、细胞生存和细胞凋亡等多个相关的下游靶基因表达。我们前期的研究发现，低氧后处理可通过通过调控HIF-1α和神经珠蛋白（neuroglobin, Ngb）蛋白表达，而对大鼠短暂全脑缺血发挥神经保护作用。但在低氧后处理作用中，HIF-1α的转录调控机制尚未完全清楚；且在该作用中，HIF-1α与Ngb是否存在关联目前亦未见报道。本项目拟在成年大鼠短暂全脑缺血低氧后处理模型上，采用免疫组化、免疫荧光、免疫印迹、慢病毒载体构建、凝胶迁移、染色质免疫共沉淀等方法，探讨在低氧后处理脑保护作用中，HIF-1α的转录调控机制，及其对Ngb表达的影响。

Hypoxia inducible factor-1 α(HIF-1α), a crucial regulator of the response to hypoxia. HIF-1α binds to hypoxia-response elements and activates the transcription of hundreds of genes involved in diverse processes such as metabolic reprogramming, angiogenesis, cell survival and apoptosis, in response to hypoxia. Our previous researches demonstrate that hypoxic postconditioning mediated neuroprotection against transient global cerebral ischemia through regulating HIF-1α and neuroglobin (Ngb). However, the transcriptional regulation mechanism of HIF-1α and the relationship between HIF-1α and Ngb are still unclear. Hence, the purpose of this study is to explore the transcriptional regulation mechanism of HIF-1α and the influence on express of Ngb in the hypoxic postconditioning-mediated neuroprotection by immunohistochemistry, immunofluorescence, immunoblotting,lentivirus construction, EMSA, and ChIP.