缺血后适应(ischemic postconditioning)显著减轻心跳呼吸骤停/复苏等引起的急性低氧缺血性脑损伤,根据实施时间、部位可分为快速和延迟后适应、原位和远端后适应。本文重点综述了缺血后适应的神经保护机制,涉及维持氧化还原平衡、调节自噬系统稳态和能量代谢稳态、减轻全身炎症反应及抑制泛死亡等环节,通过多途径、多靶点分子网络减轻低氧缺血性脑损伤。缺血后适应有望成为急性低氧缺血性脑病临床治疗的新措施,并为多机制靶向药物的研发提供新思路。

Ischemic postconditioning significantly attenuates acute hypoxic-ischemic brain injury caused by cardiopulmonary arrest followed by resuscitation, which can be further divided into rapid and delayed postconditioning, as well as in situ and remote postconditioning, according to the time and location of implementation. This review focuses on the molecular mechanisms underlying the neuroprotective effects of ischemic postconditioning, involving the maintenance of redox balance, regulation of autophagy and energy metabolism homeostasis, reduction of systemic inflammatory responses, as well as suppression of PANoptosis, thus reducing hypoxic-ischemic brain injury through multi-pathway and multi-target molecular networks. Ischemic postconditioning is expected to be a new approach for the clinical treatment of acute hypoxic-ischemic encephalopathy, providing new perspectives for the development of multi-targeting drugs.