跑台训练对慢性脑缺血大鼠海马区Notch1和突触素表达的影响

关键词：慢性脑缺血  跑台训练  Notch1  突触素

Keywords:chronic cerebral ischemia  treadmill training  Notch1  synaptophysin

摘要：

      摘要 目的：研究跑台训练对慢性脑缺血大鼠海马区Notch1和突触素（SYN）表达的影响，从而探讨跑台训练对慢性脑缺血的康复作用及其可能的分子机制。 方法：选取雄性的SD大鼠90只，随机分为9组，3个假手术对照组（7d、14d、28d）、3个模型组（7d、14d、28d）和3个跑台训练组（7d、14d、28d），每组10只。采用双侧颈总动脉永久性结扎法制备慢性脑缺血模型，假手术组仅分离双侧颈总动脉不结扎。跑台训练组于术后第3天开始跑台训练，1周训练6d。在各个时间点，应用Western-blot和免疫组化分析各组大鼠海马区Notch1和突触素表达的变化情况。 结果：与同时段的假手术组相比较，模型组和跑台训练组海马组织Notch1蛋白含量和表达在28d时都发生明显降低（P＜0.05）；其中，模型组对比跑台组降低更为明显（P＜0.05）。模型组和跑台训练组较假手术组突触素（synaptophysin，SYN)蛋白含量和表达也发生降低。其中，跑台训练组Notch1和SYN蛋白含量和表达在28d时要明显高于模型组（P＜0.05）。 结论：跑台训练可以增加慢性脑缺血大鼠海马区Notch1和突触素的表达。

Abstract:

      Abstract Objective: To investigate effects of treadmill training on the expression of Notch1 and synaptophysin in the hippocampus of rats with chronic cerebral ischemia. Method: Ninety male SD rats (250—300g) were randomly divided into nine groups including three sham groups (7 days, 14 days and 28 days), three model groups (7 days, 14 days and 28 days) and three treadmill training groups (7 days, 14 days and 28 days). N=10 for each group. The chronic cerebral ischemia models in both model groups and treadmill training groups were prepared by ligating bilateral common carotid artery permanently， while the sham groups only isolated bilateral common carotid artery without ligation. Treadmill training started at the third day after surgery with six days training for every week. At different time points, analyzing the expression level of Notch1 and synaptic in hippocampus by immunohistochemical staining and Western Blot test. Result:The expression of both Notch1 and SYN proteins in rats of sham groups were significantly higher than those in the rats of both model groups and treadmill training groups on day 28（P＜0.05）,while the expression of both Notch1 and SYN proteins in treadmill training groups were significantly higher than those in the rats of the model groups on day 28（P＜0.05）. Conclusion: Treadmill training could increase the expression of both Notch1 and synaptophysin in hippocampus of the rats with chronic brain ischemia.