中文摘要：

目的研究β-淀粉样蛋白（Aβ25-35）对sD大鼠脑海马细胞内Ca^2＋ -ATPase、游离钙离子浓度和线粒体膜电位的影响，探讨Aβ25-35对大鼠神经毒性作用的机制。方法将90只SD大鼠按体重随机分为6组，采用海马内注射染毒方式，剂量分别为Aβ10、5和1βg/只组，设立生理盐水组、假手术组和正常对照组。分别于术后7、14和21d处死实验大鼠，取海马检测神经细胞内Ca^2＋ -ATP活力、细胞内游离钙离子浓度和线粒体膜电位的改变。结果在术后7、14和21d时，Aβ10μg/只组海马细胞内Ca^2＋ -ATPase分别为（O．24±0．05）、（0．14±0．01）和（0．09±0．01）U／mg，显著低于生理盐水组（P〈0．01），同时具有明显的剂量．时间依赖关系；Aβ25-35可以增高细胞内Ca^2＋浓度，与生理盐水组相比，差异有统计学意义（P〈0．01），并且具有明显的剂量．反应关系与剂量一时间关系，差异有统计学意义（P〈0．01）；同时，Aβ25-35染毒组实验动物细胞内线粒体膜电位随时间延长和剂量升高而降低，差异有统计学意义（P〈0．01）；假手术组、生理盐水组与正常对照组之间各指标检测差异无统计学意义。结论Aβ25-35可以通过增加细胞内钙浓度，破坏线粒体功能而发挥神经毒性作用。

英文摘要：

Objective To study the effects of β-amyloid（Aβ25-35 ）on intra-cellular Ca^2＋ -ATPase.free calcium concentration and mitochondria membrane potential on SD rat hippocampus cells, thereby to investigate the mechanism of neurotoxicity of Aβ25-35. Methods A total of 90 SD rats were randomly divided into 6 groups（with 10.5.1 μg Aβ25-35 .normal group.physiological saline group and sham operated group）, using injection style of inner hippocampus with Aβ25-35 .Executing experimentation rats at 7 d. 14 d and 21 d respectively, then detecting the activity of Ca^2＋ -ATPase, the changes of intra-cellular free calcium and mitochondria membrane of rat cell with Fluo-3/AM and Rhodamine 123 probes. Results Compared to physiological saline group, Ca^2＋ -ATPase＇ s activity of Aβ group descended significantly following the increase of dose and the lengthen of time, but physiological saline group and sham operated group and normal group had no significant difference ; Aβ25-35 can increase intra-cellular calcium concentration and had significant difference compared to physiological saline group（ P 〈 0.01 ）, it also had significant dose-reaction relationship and dose-time relationship（ P 〈 0.01 ）, while sham operated group and normal group had no significant difference compared to physiological saline group;Meanwhile the intra-cellular mitochondria membrane of Aβ25-35 group＇s rats degraded following time＇s lengthen and dose＇s increase, also the difference had statistical significance but normal group and sham operated group had no significant difference compared to physiological saline group. Conclusion Aβ25-35 formed a neurotoxicity effect by disturbing the calcium homeostasis and the mitnchondria functions.