Akaneya Y, Takahashi M, Hatanaka H
Division of Protein Biosynthesis, Osaka University, Japan.
Neurosci Res. 1994 May;19(3):279-85. doi: 10.1016/0168-0102(94)90040-x.
We have established an in vitro hypoxia model using cultured central nervous system neurons from postnatal 4-day-old (P4) rats, in which death may be correlated with N-methyl-D-aspartate (NMDA)-related toxicity. P4 rat hippocampal and neocortical neurons in culture were prevented from death by the addition of MK-801, an NMDA receptor antagonist, and also partially by the removal of calcium ions from the medium, suggesting that NMDA receptors were associated with neuronal death in this in vitro hypoxia model. The neuronal death induced by the model was attenuated by the addition of alpha-tocopherol, indicating that free radicals emerged after hypoxia. This event seems similar to the hypoxia-reoxygenation phenomenon in in vitro hypoxia. Continuous treatment with basic fibroblast growth factor (bFGF) during hypoxia, and bFGF pretreatment for 6 h and removal before hypoxia induced the resistance to hypoxia-mediated cell death.
我们使用出生后4天（P4）大鼠的中枢神经系统培养神经元建立了体外缺氧模型，其中细胞死亡可能与N-甲基-D-天冬氨酸（NMDA）相关毒性有关。培养的P4大鼠海马和新皮质神经元通过添加NMDA受体拮抗剂MK-801得以防止死亡，并且通过从培养基中去除钙离子也能部分防止死亡，这表明在该体外缺氧模型中NMDA受体与神经元死亡相关。该模型诱导的神经元死亡通过添加α-生育酚而减弱，表明缺氧后出现了自由基。这一事件似乎类似于体外缺氧中的缺氧-复氧现象。在缺氧期间用碱性成纤维细胞生长因子（bFGF）持续处理，以及bFGF预处理6小时并在缺氧前去除，可诱导对缺氧介导的细胞死亡产生抗性。
