大鼠全脑缺血再灌注损伤及相关分子表达的时间过程  

Time course of brain damage and expression of related molecules in rats with transient global cerebral ischemia

作　　者：张丽慧[1] 魏尔清[1] 

机构地区：[1]浙江大学医学院

出　　处：《浙江大学学报（医学版）》2002年第2期77-80,85,共5页Journal of Zhejiang University(Medical Sciences)

基　　金：国家自然科学基金资助项目 (39770 2 70 )

摘　　要：目的 :研究大鼠全脑缺血再灌注损伤的时间过程及相关分子的表达变化。方法 :在四血管阻断法 (4VO)诱导全脑缺血模型上观察脑组织病理改变 ;同时应用免疫印迹方法检测脑组织 NMDA受体亚单位蛋白及 VCAM- 1水平。结果 :全脑缺血再灌注后 3～ 14 d海马 CA1区产生迟发性神经元死亡。皮层 NR1和 NR2 A亚单位表达分别于再灌注后 1和 3d显著增加 ,NR2 B亚单位在 1～ 3d也显示较高水平 ;海马 NR1亚单位表达在 1d明显下降 ,以后呈进行性升高 ,于 14 d达高峰 ;NR2 A和 NR2 B表达有相似的趋向并于 7d明显增加。海马和皮层 VCAM- 1分别于再灌注后 3和 7d表达明显上调。结论 :脑缺血再灌注过程中海马神经元数量减少 ,皮层和海马的 NMDA受体亚单位蛋白 (NR1、NR2 A和 NR2 B)及粘附分子 VCAM- 1有不同变化 ;干预两者的表达可能减轻脑缺血再灌注损伤。Objective: To investigate the time course of brain damage and the expression of related molecules during reperfusion after transient global cerebral ischemia in rats. Methods: Brain damage was induced by four vessel occlusion (4VO). After 1 14 days brain pathological changes were observed and expression of N methyl D aspartate(NMDA) receptor subunits and vascular cell adhesion molecule 1(VCAM 1) molecules in the cortex and hippocampus was measured by immunoblotting. Results: Three to fourteen days post 4VO induced global cerebral ischemia, the hippocampal CA1 region showed the delayed neuronal death. The expression of NMDA receptor su bunit 1 (NR1) and NMDA receptor subunit 2A (NR2A) in the cortex increased by the first and third day respectively; NMDA receptor subunit 2B (NR2B) expression showed high level on 1st and 3rd days. In the hippocampus, NR1 subunit expression decreased on day 1, but gradually increased thereafter and reached a peak level by the 14th day; NR2A and NR2B subunits expression similarly increased by the 7th day. VCAM 1 expression in the hippocampus and cortex increased by the 3rd and 7th days respectively. Conclusion: During reperfusion after transient global cerebral ischemia, hippocampal neuron density decreases. Peak expression of NMDA receptor subunits (NR1? NR2A?NR2B) and VCAM 1 molecules occurs according to a different time course specific to brain area, cortex vs. hippocampus. Interfering their expression may attenuate cerebral ischemia/reperfusion induced neural damage.

关 键 词：脑缺血 病理学 再灌注损伤 血管细胞粘附分子-1 N-甲基-D-天冬氨酸 免疫印迹 迟发性神经元死亡 

分 类 号：R-332[医药卫生]