Charriaut-Marlangue C, Remolleau S, Aggoun-Zouaoui D, Ben-Ari Y
Université René Descartes-INSERM U29, Paris, France.
Biomed Pharmacother. 1998;52(6):264-9. doi: 10.1016/S0753-3322(98)80012-7.
Hypoxic-ischemic neuronal death has long been considered to represent necrosis, but it now appears that many brain neurons undergo apoptosis after either global or focal ischemic insults. Recent studies demonstrated: 1) DNA cleavage into oligonucleosome-sized fragments demonstrated by a typical ladder pattern; 2) early endonuclease activation, as demonstrated by the presence of high molecular weight DNA fragments (300 to 50 kbp); 3) chromatin condensation and apoptotic bodies formation; 4) activation of apoptosis-associated proteins. These results may indicate that apoptosis contributes to the development of the ischemic infarct and is probably substantially distinct from ischemia-triggered excitotoxicity, which tends to produce necrosis.
长期以来,缺氧缺血性神经元死亡一直被认为是坏死,但现在看来,许多脑神经元在全脑或局灶性缺血损伤后会发生凋亡。最近的研究表明:1)DNA 裂解为寡核小体大小的片段,表现为典型的梯状条带模式;2)早期核酸内切酶激活,表现为高分子量 DNA 片段(300 至 50 kbp)的存在;3)染色质浓缩和凋亡小体形成;4)凋亡相关蛋白的激活。这些结果可能表明,凋亡促成了缺血性梗死的发展,并且可能与缺血引发的兴奋性毒性有很大不同,后者往往导致坏死。