SPINAL ISCHEMIA, ITS MECHANISM AND STRATEGY OF TREATMENT-A NEW MODEL AND GLIAL REACTION AND INDUCTION

1）光和电子微观定位的单链DNA蛋白，一个标志的凋亡已经研究过。免疫作用在一天后被确认为在没有形态学变化的情况下核生物。单链DNA的降级可以在延迟神经元死亡期间准确地预测双链DNA破裂的出现。（Neurosci Lett 240 ： 69， 1998）2） DDC induced apoptosis in a morphological nature in PC12 cells， and led to down-regulation of Cu/Zn-SOD activity， then reduced intracellular Hy D22 y D22 y D2。一个hypoxia从DDC诱导的凋亡中预防了细胞。These data confirmed O-D22-D2 induced apoptosis in PC12cells。氮氧化物合成酶、铁基催化剂没有预防凋亡，过氧化物酶和OH也没有对DDC诱导的凋亡产生影响。NGF和NAC保护的凋亡。DDC未激活NF-kB。我们包含NAC减少的DDC诱导的apoptosis by interception of an unknown直接信号路径，由其中的Oy D22 y D2诱导的apoptosis。

1) The light and electron microscopic localization of single strand DNA protein, a marker of apoptosis was studied. Immunoreaction was recognized in the nucleus without morphological changes 1 day after ischemic insult. Degradation of single strand DNA can occur during delayed neuronal death, preceding the appearance of double strand DNA breaks.(Neurosci Lett 240 : 69, 1998)2) DDC induced apoptosis in a morphological nature in PC12 cells, and led to down -regulation of Cu/Zn-SOD activity, then reduced intracellular HィイD22ィエD2OィイD22ィエD2. A hypoxia prevented the cells from DDC-induced apoptosis. These data confirmed OィイD22ィエD2 induced apoptosis in PC12 cells. Nitro-oxide-synthetase, Fe-chelator did not prevent the apoptosis.Peroxinitrate and also OH did not contribute DDC-induced apoptosis. NGF and NAC protected the apoptosis. DDC did not activate NF-kB. We concluded that NAC reduced DDC-induced apoptosis by interception of an unknown direct signal pathway, by which OィイD22ィエD2 induced apoptosis.