The neonatal brain is susceptible to hypoxic-ischemic injury due to its developmental characteristics. Hypoxia-ischemia means a decreased perfusion of oxygen and glucose, which can lead to severe encephalopathy. Although early initiation of therapeutic hypothermia was reported to provide neuroprotection for infants after HI, hypothermia administered alone after the acute insult cannot reverse the severe damage that already has occurred or improve the prognosis of severe hypoxic-ischemic encephalopathy. Therefore, exploring new protective mechanisms for treating hypoxic-ischemic brain damage are imperative. Until now, many studies reported the neuroprotective mechanisms of hypoxic/ischemic preconditioning in protecting the hypoxic-ischemic newborn brains. After hypoxia and ischemia, hypoxia-inducible factor signaling pathway is involved in the transcriptional regulation of many genes and is also play a number of different roles in protecting brains during hypoxic/ischemic preconditioning. Hypoxic/ischemic preconditioning could protect neonatal brain by several mechanisms, including vascular regulation, anti-apoptosis, anti-oxidation, suppression of excitotoxicity, immune regulation, hormone levels regulation, and promote cell proliferation. This review focused on the protective mechanisms underlying hypoxic/ischemic preconditioning for neonatal brain after hypoxia-ischemia and emphasized on the important roles of hypoxia inducible factor 1 signaling pathway.

中文翻译：

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缺氧缺血性损伤新生儿脑缺氧/缺血预处理的神经保护作用。


由于其发育特点，新生儿大脑很容易受到缺氧缺血性损伤。缺氧缺血意味着氧气和葡萄糖的灌注减少，这可能导致严重的脑病。尽管据报道早期开始治疗性低温可为脑损伤后的婴儿提供神经保护，但在急性损伤后单独实施低温不能逆转已经发生的严重损伤或改善严重缺氧缺血性脑病的预后。因此，探索新的治疗缺氧缺血性脑损伤的保护机制势在必行。迄今为止，许多研究报道了缺氧/缺血预处理对保护缺氧缺血新生儿大脑的神经保护机制。缺氧、缺血后，缺氧诱导因子信号通路参与多种基因的转录调控，在缺氧/缺血预处理过程中发挥多种不同的保护大脑的作用。缺氧/缺血预处理可通过多种机制保护新生儿脑，包括血管调节、抗凋亡、抗氧化、抑制兴奋性毒性、免疫调节、激素水平调节、促进细胞增殖等。本文重点阐述了缺氧/缺血预处理对新生儿脑缺氧缺血后的保护机制，并强调了缺氧诱导因子1信号通路的重要作用。