脓毒症性脑病(SAE)是临床重症监护病房中常见脑病之一，对患者的预后影响极大，目前尚无特异性治疗方案。我们前期研究发现，脑红蛋白(Ngb)表达上调是神经系统自我保护机制中重要的组成部分，脑红蛋白与脓毒症性脑病预后负相关。然而在SAE中Ngb仅在早期短暂表达，不能达到持续保护。结合前期研究和文献，我们提出Ngb甲基化或表达量不足可能是抑制Ngb持续表达的重要因素。同时Ngb不仅能抑制神经元的凋亡达到保护作用，还可能通过诱导线粒体的自噬作用，促进损伤神经元修复。为了验证上述假说，我们采用细胞缺氧缺血模型和动物SAE模型，研究Ngb的时空表达特征；通过去甲基化和过表达Ngb方法，观察对脓毒症性脑损伤的持续保护作用；并进一步通过干预线粒体自噬作用，观察其对Ngb保护作用的影响。从三个层次全面研究Ngb在SAE中的作用及调控机制，为寻找更佳的调控Ngb表达，甚至为开发Ngb类似物提供新的切入点。

Sepsis associated encephalopathy (SAE) is one of the most common cerebropathy in intensive care unit with huge impact on patients’ prognosis. There is no specific treatment for SAE now. In our previous research, Neuroglobin (Ngb) is negative-correlated with prognosis of SAE, and the up-regulation of Ngb expression plays an important role in self-protection of the nervous system. However, Ngb is only expressed in early stage of SAE and could not offer continuous protection. We hypothesize that methylation of Ngb is an important factor of inhibiting Ngb expression, meantime, Ngb could protect nervous system through restraining apoptosis of neurons and inducing autophagy of mitochondria to improve repair of damaged neurons. To prove that, we use hypoxic-ischemic cell model and SAE animal model to study the spatiotemporal characteristics of Ngb expression. Also we observe the protection effect of Ngb by intervening expression and demethylation of Ngb. Furthermore, we investigate the impact on protection effect of Ngb by interfering the autophagy of mitochondria. We use the three points to comprehensively study Ngb in SAE, look for better regulation of Ngb expression, and offer new viewpoint for Ngb-like medicine.