大脑尤其是海马对缺血异常敏感，而突破脑缺血后神经保护治疗的困境是当今卒中研究中的重大课题。脑红蛋白（Ngb）是一种潜在的神经保护剂。我们通过预实验证实，低氧后处理可使大鼠短暂全脑缺血后海马CA1区Ngb和Na+-K+-ATP酶（NKA）β1亚基表达增加，然而低氧后处理通过怎样的调控机制影响Ngb及其下游的？我们的研究也表明低氧后处理通过上调CA1区低氧诱导因子1α（HIF-1α）的表达，对脑缺血发挥保护作用。由此我们提出如下假说：低氧后处理通过上调CA1区HIF-1α，进而上调Ngb，维持NKA β1和β2亚基的表达；另外，上调的Ngb可降低氧化应激水平，减轻线粒体损伤和抑制NKAβ1和β2亚基谷胱甘肽化，进而维持NKA活性，减少细胞凋亡，发挥神经保护作用。本研究拟应用分子生物学技术，确定Ngb在脑缺血后低氧后处理神经保护中的分子机制，为确立Ngb作为脑缺血治疗的靶点提供更充分的科学依据。

Pyramidal neurons in hippocampal CA1 regions are highly sensitive to cerebral ischemia. A complete understanding of the neuroprotective molecule mechanisms against cerebral ischemic injury is regarded as an urgent and critical research topic. Neuroglobin (Ngb) is a newly discovered globin that is widely expressed in the central nervous systems. Its high affinity for oxygen and preferential expression in cerebral neurons imply a possible role in neuroprotection against neuronal hypoxia and cerebral ischemia. In preliminary studies we demonstrated that hypoxic postconditioning (HPC) significantly increased the expressions of Ngb and Na+-K+-ATPase (NKA) β1 in the hippocampal CA1 subregion after transient global cerebral ischemia (tGCI). However, the molecular mechanisms of Ngb neuroprotection induced by HPC remain poorly understood. Furthermore, our previous studies showed that over-expression of hypoxia-inducible factor (HIF)-1α in the hippocampal CA1 subregion contributed to HPC-mediated neuroprotection against tGCI. Therefore, we hypothesized that over-expression HIF-1α induced by HPC can up-regulate Ngb and NKA β1 and β2 subunits in the hippocampal CA1 subregion. Also, Ngb overexpression induced by HPC significantly reduced tGCI-mediated mitochondria damage, ROS release, and NKA β1 and β2 subunits glutathionylation, which in turn maintains the activation of NKA and decreases neuron apoptosis in the hippocampal CA1 subregion after tGCI. More insights will be obtained on the neuroprotective molecular mechanisms of Ngb induced by HPC. Moreover, in a context of cerebral ischemia a complete understanding of the mechanisms regulating neuronal damage might provide new targets for the therapy of ischemic stroke.