新生儿缺氧缺血性脑病的机制研究和治疗新进展

New Progress in Mechanisms and Therapeutic Strategies of Neonatal Hypoxic-Ischemic Encephalopathy

新生儿缺氧缺血性脑病(HIE)是指由于围产期窒息后缺氧导致的脑缺氧缺血性损害,是造成新生儿死亡和婴幼儿神经功能障碍的主要原因。虽然新生儿重症监护室(NICU)在生命支持治疗方面取得了巨大的进展,但HIE带来的严重后果包括死亡、脑瘫、癫痫以及其他显著的认知、发育和行为障碍等问题的发生率仍然很高,给病人、家庭和社会带来了沉重的负担。近年来,国内外研究者们从动物模型和人类婴儿着手,开展了大量有关HIE的分子机制和相应治疗靶点的研究。本文将在讨论传统治疗策略的基础上,进一步就近年来国内外缺氧缺血性脑损伤(HIBD)的主要细胞和分子机制及新的治疗策略作一综述,以期为HIE的临床治疗提供参考。

Neonatal hypoxic-ischemic encephalopathy（HIE）is a kind of hypoxic-ischemic brain damage（HIBD）induced by hypoxia after perinatal asphyxia,which is a major cause of death and neurologic disability in children.Although tremendous progress has been made in providing life-support therapy in neonatal intensive care unit,the incidence of serious consequences including death,cerebral palsy,epilepsy and other cognitive,developmental and behavioral problems remains high.Therefore,it places a large burden on patients,their families,and society.In recent years,extensive researches on molecular mechanisms and potential therapy targets of HIE have been performed in experimental animals and human infants.Based on the traditional treatment strategies,this review will focus on the recent advances in the main cellular and molecular mechanisms of HIBD and new therapeutic strategies,which can provide reference for the clinical treatment of HIE.