新生儿脑细胞缺氧缺血后主要死因为凋亡。Bax依赖性的线粒体外膜通透性增加使位于线粒体内膜的促凋亡因子,如细胞色素C、凋亡诱导因子释放入胞质。细胞色素C通过激活Caspase9/3导致DNA断裂,凋亡诱导因子和亲环素A结合引起染色质溶解。阻断线粒体外膜通透性增加有可能成为围生期脑损伤后神经保护的重要措施。 Neonatal brain cells after hypoxia and ischemia the main cause of death is apoptosis. Bax-dependent increase in mitochondrial outer membrane permeability causes release of pro-apoptotic factors, such as cytochrome C and apoptosis-inducing factor, located in the mitochondrial inner membrane. Cytochrome C causes DNA cleavage by activation of Caspase9 / 3, which induces chromatin lysis by binding of the apoptosis-inducing factor and cyclophilin A. Blocking the increase of mitochondrial outer membrane permeability may become an important measure of neuroprotection after perinatal brain injury.