中文摘要：

目的：观察突触后密度（PSD）-93基因在大鼠局灶性脑缺血再灌注皮质表达的变化。探讨其在缺血再灌注损伤中的病理作用。方法：线栓法建立大鼠大脑中动脉闭塞再灌注模型，缺血2h后，分别再灌注6、12和24h，应用RT—PCR、Western blot技术检测缺血再灌注后皮质PSD-93基因mRNA和蛋白的表达。结果：缺血再灌注的非缺血侧大脑皮质PSD-93 mRNA和蛋白的表达与对照组相比均无明显变化；缺血侧皮质PSD-93 mRNA表达明显高于未缺血侧，12、24h组与未缺血侧比较具有显著性差异（均P〈0.05），并呈时间依赖性；再灌注6h后PSD-93蛋白表达升高，再灌注12h达高峰，12h组与未缺血侧比较具有显著性差异（P〈0．05）。结论：脑缺血再灌注后皮质PSD-93基因表达增高，推测PSD-93参与介导缺血性脑损伤。

英文摘要：

Objective To investigate the expression and pathological function of postsynaptic density-93 （PSD-93 ） after rat focal ischemic middle cerebral artery occlusion/reperfusion （MCAO）. Methods After the fight middle cerebral artery occluded for 2 hours,the rats were reperfused for 6,12 and 24 h before decapitation. PSD-93 gene and protein in the cortex were measured by reverse transcription polymerase chain reaction （RT-PCR） and Western blot. Results There were no differences of the expression of PSD-93 between the sham operation-group and the non-ischemic sides ;PSD-93 mRNA gradually increased, and the expressions on the ischemic sides were higher than that on the non-ischemic sides.The expressions of 12,24 h groups were increased significantly （P 〈 0.05 ） in a time-dependent manner;PSD-93 protein expression level increased at 6 h and reached the peak at 12 h, showing a significant difference at 12 h （ P 〈 0. 05 ）. Conclusions These results indicate that PSD-93 gene expression may be up-regnlated after reperfusion following focal cerebral ischemia. And this change may be involved in the pathogenesis of focal cerebral ischemia.