β-淀粉样蛋白与载脂蛋白E4对大鼠海马突触素的影响

目的观察β-淀粉样蛋白（Ap）和载脂蛋白E（apoE）4对大鼠海马突触素（synaptophysin，SYN）的影响以及二者是否具有协同作用。方法将24只雄性Wistar大鼠分为4组：对照组海马注射生理盐水，n13组注射Aβ1-40，apoFA组注射apoE4，Aβ＋apoFA组注射Aβ1-40＋apoFA。15d后水迷宫检测各组大鼠的学习记忆能力，之后免疫组化法检测CA1区突触素的表达。结果apoE4组、Ap组与对照组比较大鼠第5天的逃避潜伏期明显延长，跨台次数明显减少（P〈0．01）；AB组与apoE4组比较，大鼠第5天的逃避潜伏期明显延长，跨台次数明显减少（P〈0．01）；AB与apoFA之间存在交互作用（F=7．098，P〈0．01）。apoE4组、A13组比对照组突触素OD值下降明显（P〈0．01）；Ap组比apoFA组下降明显（P〈0．05）；Aβ＋apoE4组比对照组、apoFA组及Ap组均下降明显（P〈0．01）；Aβ与apoFA具有交互作用（P〈0．05）。结论Aβ及apoE4均可损伤海马突触结构；A13对海马突触结构损伤比apoE4严重。Aβ与apoFA对海马突触结构的损伤具有协同作用。

Effects of beta-amyloid protein and apoE4 on hippocampal synaptophysin in rats

Objective To investigate the effects of beta-amyloid protein（AI3） and apoE4 on synaptophysin（SYN） in hippocampus and their synergistic effect. Methods Twenty-four male Wistar rats were divided into four groups：control group, Aβ group, apoE4 group and Aβ ＋ apoE4 group. Normal saline,Aβ ,apoE4 and Aβ ＋ apoE4 were respectively injected in four groups under the control of a brain stereotaxic apparatus. The Morris water maze test was performed at 15 d,then the expression of SYN in hippocampus CA1 regions was detected. Results Through 5 d training,the escape latency of all rats shortened gradually. Compared with control group,the es- cape latencies were significantly prolonged in Aβ group and apoE4 group at 5 d（ P 〈 0.01 ）, and the times of passing platform were decreased（ P 〈 0.01 ）. Compared with apoE4 group, the escape latencies were significantly prolonged in AI3 group at 5 d（ P 〈 0.01 ） , and the times of passing platform was decreased （ P 〈 0. 01 ）. An interaction between AI3 and apoE4 also was observed （ F = 7. 098, P 〈 0.01 ）. Optical density of synaptophysin was significantly lower in AI3 group and apoE4 group than in control group（ P 〈 0.01 ）. Optical density of synaptophysin was significantly lower in AI3 ＋ apoE4 group than in the other three groups（P 〈0. O1 ）. A3 and apoE4 had an interaction in lowering optical density value of synaptophysin（P 〈 0.05）. Conclusion AI3 and apoFA all could induce the injury to hippocampal synapse formation, and AI3 could induce more serious injury than apoE4. Aβ and apoE4 have synergistic effect in this injury course.