摘要
据报道,脑缺血损伤能导致迟发性神经元死亡(delayedneuronaldeath,DND)。有学者认为DND是神经兴奋毒性作用引起的细胞坏死过程,也有学者认为主要是凋亡机制参与了DND。我们研究发现,大鼠全脑缺血15min后再灌流48h,海马CA1区锥体细胞大量死亡,其超微结构出现细胞膜完整的胞浆浓缩和核固缩的凋亡样形态学改变,并且蛋白合成抑制剂放线菌酮对CA1区锥体细胞的脑缺血损伤具有明显的保护作用。说明脑缺血后锥体细胞的死亡需要一定的时间合成新的蛋白质,从而激活细胞内部死亡程序。提示凋亡机制参与全脑缺血后DND。
AbstractAbstract:It was reported that ischemia induced delayed neuronal death(DND).Some authors consider DND as necrosis mediated by excitotoxicity,others consider apoptosis contributes importantly to DND.Our present work demonstrates a lot of pyramidal cells of CA1 region in hippocampus will die 48 h after reperfusion following 15 min global ischemia in rats.The ultrastructure of these pyramidal cells shows apoptosislike changes with condensed cytoplasm, pyknotic nucleus and intact cytomembrane. Furthermore the protein synthesis inhibitorcycloheximide could prevent CA1 pyramidal cells from DND remarkably,which implies a certain time will be required after ischemia for pyramidal cells to synthesize new proteins to activate the cellular death program.It suggests that apoptosis may be involved in DND following global ischemia. KEY WORDS ischemia; DND; hippocampus; apoptosis; ultrastructure; cycloheximide
出处
《中国应用生理学杂志》
CAS
CSCD
1998年第3期201-204,共4页
Chinese Journal of Applied Physiology
基金
国家自然科学基金
广东省自然科学基金