中文摘要：

目的：观察大鼠在局灶性脑缺血早期脑组织内血管生成素（Ang）-1和Ang-2mRNA在不同时间点的表达变化，探讨其变化规律并分析脑缺血后Ang-1、Ang-2在缺血性脑卒中发病中的作用机制。方法：大鼠随机分为正常对照组（C组）、假手术组（S组）和缺血组（I组），缺血组又分为缺血1、3、6、12、24、48和72h组，采用改进的线栓法制做永久性大脑中动脉闭塞（MCAO）模型，采用RT—PCR技术检测各组大鼠脑组织缺血半影区内Ang-1 mRNA及Ang-2 mRNA的表达水平。结果：正常对照组和假手术组Ang-1 mRNA中等量表达，两组表达量比较差异无显著性（P〉0．05）；Ang-2 mRNA极低量表达，两组表达量比较差异无显著性（P〉0．05）；缺血组Ang-1 mRNA表达水平在脑缺血早期（3～6h）低于C组（P〈0．01），脑缺血48～72h高于C组（P〈0．01）；Ang-2 mRNA在脑缺血后3h表达水平高于C组，在脑缺血后12h出现高峰，且持续至脑缺血后72h（P〈0．01）。结论：Ang-1和Ang-2可能在局灶性脑缺血后与其他血管特异性生长因子共同参与缺血半影区的新血管形成并抑制神经元细胞凋亡，有利于改善缺血半影区血液供应和促进神经功能恢复。

英文摘要：

Objective To investigate the changes of expressions of angiogenin-1 （Ang-1） and -2 mRNA in the ischemic brain at different time points, find their regularities and discuss their mechanisms of action after cerebral ischemic stroke. Methods All the rats were divided into 3 groups： control group （group C）, sham-operation group （group S）, and ischemia group （group I）. Rats in group I were divided into 7 subsets, they were 1, 3, 6, 12, 24, 48 and 72 h after middle cerebral artery occlusion （MCAO） （n=7 per time point）. The mRNA levels of Ang-1 and Ang-2 were measured by reverse transcription polymerase chain reaction （RT-PCR）. Results In the brain tissues of the rats in group C and group S, the expression levels of Ang-1 mRNA were moderate, the expression levels of Ang 2 mRNA were extremely low, there were no significant differences between two groups （P〉0.05）. In group I, the mRNA levels of Ang-1 were lower than those in group C during 3-6 h after onset of isehemia （P〈0. 01）, and were higher than those in group C during 48-72 h after MCAO （P〈0.01）. After MCAO, the expression level of Ang 2 mRNA was higher than that in group C at 3 h after onset of ischemia, the level peak at 12 h, and last for up to 72 h after ischemia （P〈0.01）. Conclusion Ang-1, Ang-2 and other specific vessel growth factors may regulate the process of vessel formation together after focal cerebral ischemia, they can enhance blood flow, restrain neuron apoptosis in ischemic penumbra, and promote nerve function to recover.