Abstract: Apoptosis is involved in the pathological process of hypoxic-ischemic braindamage. Once hypoxia-ischemia occurs, a number of independent pathways can lead to apoptosisrespectively. The mitochondrial pathway attached increasing attention. A variety of factorspromoting and anti-apoptotic play roles in the mitochondria, triggering mitochondrial functionand biochemical changes, and determining the fate of cells after injury. The key processs ofmitochondrial pathways include the generation of apoptotic stimulator, changes in mitochondrialpermeability, release of mitochondrial apoptotic factors, caspase family activation, and so on.Ifthey can be blocked on the above processes, excessive apoptosis of neurons can be inhibited andthe hypoxic-ischemic brain injury will be reduced. Clinical research and animal experiments haveconfirmed that hyperbaric oxygen therapy can reduce neuronal apoptosis. However, the mechanismis so complex that it is not yet completely clear. This article will explore the possible mechanism ofhyperbaric oxygen therapy for mitochondrial pathways of apoptosis.

Key words: Hyperbaric oxygenation; Apoptosis; Mitochondria

摘要： 凋亡参与了缺血缺氧性脑损伤后的病理过程，当发生缺血缺氧后，有多条通路可以分别独立地引发细胞凋亡，其中的线粒体途径越来越受到重视,在线粒体内，存在多种促凋亡和抗凋亡因素，可以引发线粒体功能和生化方面的改变，从而决定细胞损伤后的命运。线粒体凋亡途径的主要环节有凋亡刺激物的生成，线粒体通透性的改变，线粒体凋亡因子的释放，caspase家族的激活等，如果能对上述环节加以阻断，则可抑制神经元的过度凋亡从而减轻缺血缺氧性脑损伤。临床研究及动物实验均证实高压氧治疗可以起到减轻神经元凋亡的作用，但因其作用机制复杂，故尚未完全明确，本文就高压氧治疗对线粒体凋亡途径的可能机制做一探讨。

关键词: 高压氧; 细胞凋亡; 线粒体