中文摘要：

目的观察bcl-xl基因的过表达对小鼠大脑中动脉栓塞的保护作用。探讨其作用机制。方法通过建立bcl-xl转基因小鼠，经传代及检测后证实，该转基因小鼠中存在着bcl-xl基因的过表达，然后将该模型小鼠与同种系野生型小鼠同时行线栓永久性阻塞大脑中动脉，在缺血24h时测其神经功能评分，观察转基因小鼠与野生型小鼠的差别。在缺血后不同时间点测其梗死体积，观察梗死体积的动态变化。用TUNEL法观察小鼠的脑组织缺血后不同时间点再灌注时凋亡细胞的数量和分布情况。用免疫组化方法观察梗死前后两种小鼠脑组织中bcl-xl的表达量的差异。结果缺血24h后转基因小鼠的神经功能评分低于野生型小鼠（P〈0．05）。缺血后3、24、72h，转基因小鼠的梗死体积均明显低于野生型小鼠，差异有显著性意义。TUNEL显示在缺血再灌注后的不同时间点。转基因小鼠皮质缺血区内的凋亡细胞数明显少于野生型小鼠，差异有显著性意义。免疫组化结果显示，梗死前后转基因小鼠的皮质细胞bcl-xl的表达量均明显高于野生型小鼠（P〈0．05），且梗死后两种小鼠体内的bcl-xl的表达量均较梗死前增加（P〈0．05）。结论在规范化的标准条件下。转基因小鼠中bcl-xl基因的过表达能够降低脑梗死的体积井改善小鼠的神经功能；过表达bcl-xl基因的这种效应可能是通过抑制细胞凋亡而实现的。

英文摘要：

Objective To study the protective effects of the over-expression of bcl-xl gene on transgenic mice following permanent occlusion of middle cerebral artery and the possible mechanism. Methods Transgenic mice and wild type mice were subjeced to intraluminal occlusion of the middle cerebral artery. The neurological outcomes were evaluated 24 hrs later. The infarct volume at different times after occlusion were measured. The apoptosis of neuron was measured by TUNEL. The expression of bcl-xl before and after occlusion was detected with immunohistochemistry. Results The neurological function scores in transgenic mice were significantly lower than those in the wild type ones （P 〈 0.05 ）. The number of neuron apoptosis in transgenic mice was significantly less than that in mild type mice （ P 〈 0.05 ）. The infarct volume of the transgenic mice was much less than that of the wild type mice at 3, 24 and 72 hrs after iscbemia （P 〈0.05）. The bcl-xl expression increased after ischemia in transgenic mice and wild mice, but the bcl-xl expression was higher in transgenic mice before and after brain ischemia than that in the wild type mice （ P 〈 0.05 ）. Conclusions Over-expression of bcl-xl can significantly reduce the infarct volume and improve neurological function in transgenic mice, possibly through inhibiting the apoptosis of neuron.