大鼠全脑缺血再灌注损伤及相关分子表达的时间过程

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3－14d海马CA1区产生迟发性神经元死亡。皮层NR1和NR2A亚单位表达分别于再灌注后1和3d显著增加，NR2B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14d达高峰；NR2A和NR2B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、NR2A和NR2B）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。

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

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.