Gwag B J, Lobner D, Koh J Y, Wie M B, Choi D W
Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Neuroscience. 1995 Oct;68(3):615-9. doi: 10.1016/0306-4522(95)00232-8.
Mouse cortical cell cultures exposed to transient oxygen-glucose deprivation developed marked acute cell body swelling followed by neurodegeneration, consistent with necrosis-type death. This death was not attenuated by the protein synthesis inhibitor, cycloheximide, but was attenuated by addition of the N-methyl-D-asparate antagonist, MK-801 (dizocilpine maleate), and the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione. If the deprivation insult was extended to overcome the protective effect of glutamate antagonists, neuronal death resulted that was associated with cell body shrinkage and DNA fragmentation, and was attenuated by cycloheximide. These data suggest that oxygen-glucose deprivation can induce in cortical neurons both excitotoxic necrosis, and apoptosis dependent on new macromolecule synthesis.
暴露于短暂氧糖剥夺的小鼠皮质细胞培养物会出现明显的急性细胞体肿胀，随后发生神经退行性变，这与坏死型死亡一致。这种死亡并未被蛋白质合成抑制剂环己酰亚胺减弱，但通过添加N-甲基-D-天冬氨酸拮抗剂MK-801（马来酸二氮卓西平）和α-氨基-3-羟基-5-甲基-4-异恶唑丙酸/海人藻酸拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮而减弱。如果延长剥夺损伤时间以克服谷氨酸拮抗剂的保护作用，就会导致神经元死亡，这种死亡与细胞体收缩和DNA片段化有关，并且会被环己酰亚胺减弱。这些数据表明，氧糖剥夺可在皮质神经元中诱导兴奋性毒性坏死和依赖新大分子合成的凋亡。
