β―淀粉样蛋白增加Wistar大鼠癫痫发作易感性行为学研究.docVIP

β―淀粉样蛋白增加Wistar大鼠癫痫发作易感性行为学研究 　　[摘要] 目的 研究β-淀粉?拥鞍祝?Aβ）对癫痫（EP）发病机制的影响。 方法 按随机数字表法将40只6～8周Wistar大鼠分为Aβ1-42+PILO组、Aβ1-42组、PBS+PILO组、PBS组，每组各10只；前两组合称为Aβ1-42模型组，后两组合称为PBS对照组。采用脑立体定位仪在Aβ1-42模型组大鼠海马CA3区注入Aβ1-42，PBS对照组给予相同剂量的PBS。2周后观察大鼠Morris水迷宫实验，记录逃避潜伏期、目标象限内游泳时间比例和穿越平台次数，检测大鼠AD模型是否成功。建模成功后通过腹腔（IP）注射氯化锂-匹罗卡品（LI-PILO）制备大鼠慢性EP模型，依据Racine分级标准，记录EP发作潜伏期、发作程度和死亡率。 结果 Aβ1-42模型组和PBS对照组各有1只大鼠死亡。Morris水迷宫实验数据分析结果，Aβ1-42 模型组与PBS对照组大鼠相比，逃避潜伏期显著延长（P 0.01），目标象限内游泳时间比例缩短（P 0.05），穿越平台次数显著减少（P 0.05），表明AD模型制备成功。制备大鼠EP模型：依据Racine分级标准，Aβ1-42+PILO组与PBS+PILO组相比，EP发作潜伏期显著缩短（P 0.01），发作程度更重（P 0.05）；Aβ1-42+PILO组与PBS+PILO组相比死亡率显著增加（P 0.05）。 结论 通过海马CA3区注射Aβ1-42，可以导致大鼠出现与海马有关的学习和记忆功能受损。在Aβ存在的基础上诱导大鼠出现EP发作的易感性增加。 　　[关键词] β-淀粉样蛋白；癫痫；阿尔茨海默病；易感性 　　[中图分类号] R73 [文献标识码] A [文章编号] 1673-7210（2017）09（c）-0025-05 　　[Abstract] Objective To study the effects of β-amyloid protein （Aβ） on the pathogenesis of epilepsy （EP）. Methods 40 male Wistar rats were divided into Aβ1-42 + PILO group， Aβ1-42 group， PBS + PILO group and PBS group by random number table， with 10 rats in each group. The former two groups were called Aβ1-42 model group and the later PBS control group. Aβ1-42 and same volume PBS were injected into the hippocampal CA3 region of Wistar rats in Aβ1-42 model group and PBS control group by stereotaxic apparatus respectively， and the Morris water maze test was observed after 2 weeks. Escape latency， the percentage of swimming time in the target quadrant and the number of times of crossing the platform were recorded. After the AD model was successfully made， the rat model of chronic EP was established by intraperitoneal injection of LI-PILO. The latency of EP， degree of seizure and mortality of rats were recorded according to Racine grading criteria. Results One rat died in Aβ1-42 model group and the PBS control group. The results of Morris water maze test showed that compared with the PBS control group， the escape latency of the Aβ1-42 model group was longer （P 　　[Key words] Beta amyloid prot