中文摘要：

目的研究Notch通路在局灶性缺血性脑卒中大鼠海马的动态变化，探讨该通路对缺血性卒中后内源性神经前体细胞再生的调控作用。方法以大脑中动脉闭塞（middlecerebralarteryocclusion，MCAO）法建立大鼠局灶性脑缺血模型，通过Westernblotting法以及Real—limeRT—PCR法，于术后19d、28d检测海马Notch通路下游靶基因Hes1、Hes5的蛋白和mRNA表达。结果术后19d，MCAO组Hes1、Hes5蛋白及mRNA表达均分别高于对照组，差异有统计学意义（P〈0．01，P〈0．05），28d时MCAO组Hes1、Hes5的蛋白及mRNA表达下降，较之对照组差异有统计学意义（均P〈0．05），而且低于19d时Hes1、Hes5的表达，差异有统计学意义（均P〈0．01）。结论卒中后的内源性神经再生机制中可能有Notch通路活性动态变化的机制参与，卒中后期Notch通路活性的显著下调可能是促进增殖的神经前体细胞向神经元方向分化的重要分子机制。

英文摘要：

Objective To detect the expression changes of Hes I and Hes 5 in the hippocampus of focal ischemic rats and explore whether the Notch pathway is involved in the endogenous repair mechanisms of central nervous system after the ischemic stroke. Methods We investigated the expression of Hes 1 and Hes 5 in the adult rat hippocampus on the 19th day and 28th day after middle cerebral artery occlusion. Data was analyzed using two-way ANOVA. Results Compared with the control groups, the protein and mRNA expressions of Hes 1 and Hes 5 were significantly up-regulated on 19th day and down-regulated on 28th day （P 〈 0.01 ）. Conclusions The down-regulation of Hes 1 and Hes 5, the Notch pathway genes, in late-stage of ischemic stroke is probably one of the endogenous repair mechanisms of the central nervous system, which promotes differentiation of the proliferated neural progenitor cells towards the neurons.