EPO对Aβ_(1-42)所致AD样大鼠空间记忆的影响及作用机制

Effects of rHu-EPO on Spatial Memory in Rats with Aβ_(1-42) Induced Alzheimer Disease and Its Mechanism

目的探讨erythropoietin(EPO)对Aβ1-42所致AD样大鼠空间记忆的影响及作用机制。方法 48只雄性Wistar大鼠随机分成4组:生理盐水对照组、AD模型组、rHu-EPO治疗组与脑复康阳性对照组,每组12只。通过海马注射Aβ1-42的方法建立模型组,rHu-EPO治疗组与脑复康阳性对照组在建立模型的基础上,分别给予腹腔注射rhEPO(5000IU/kg,隔日一次)和脑复康(40 mg/kg,每日一次)。术后第八天开始对各组进行Morris水迷宫空间记忆能力测试,使用Western blot技术检测各组大鼠synapsin1蛋白水平。结果与生理盐水组、rHu-EPO治疗组及脑复康组相比,AD组水迷宫测试潜伏期延长,synapsin1表达降低,差异均有统计学意义(P<0.05)。EPO治疗组与脑复康组相比,水迷宫测试结果与synapsin1蛋白表达差异无统计学意义(P>0.05)。结论 EPO可以显著改善AD样大鼠的空间记忆能力,其机制可能与提高synapsin1蛋白表达有关。

Objective To explore the effects of erythropoietin （EPO） on the spatial memory in AD rats induced by Aβ1-42 and its mechanism. Methods 48 Wistar male rats were randomly divided into 4 groups：saline group, AD model group , rHu-EPO treatment group and Piracetam treatment group. The AD models were established by injection of Aβ1-42 into the hippocampus, rHu-EPO treatment group was intraperitoneal injeced 5 000IU/kg rHu-EPO after the success of model making, every other day. Piracetam treatment group was intraperitoneal injeced 40 mg/kg piracetam after the success of model making, every day. The spatial memory ability of the rats were tested with Morris water maze. The protein level of synapsinl was detected by western blotting. Results AD model group showed significantly longer latency than that of all the other three groups. The expression of synapsin 1 in the rHu-EPO treatment group was significantly higher than that in the AD model group （ P 〈 0.05 ） ; While no significant differences between the rhu-EPO treatment group and Piracetam treatment group were found （P 〉 0.05 ）. Conclusion rhu- EPO can improve the spatial memory ability of AD rats induced by Aβ1-42 through increasing the expression of synapsinl.