中文摘要：

目的建立β-淀粉样蛋白1-42（Aβ1-42）致Wistar大鼠阿尔茨海默病（AD）模型,探讨二氮嗪干预后大鼠行为学及其相关凋亡因子表达的变化。方法大鼠双侧侧脑室注射Aβ1-42两周后诱导建立AD模型,部分大鼠同时注射二氮嗪干预。通过Y型迷宫电刺激评价大鼠学习和记忆能力,采用蛋白电泳方法检测大鼠大脑皮层和海马部位神经细胞内凋亡因子（Bcl-2）、半胱天冬氨酸蛋白酶-3（Caspase-3）表达水平的变化。结果与正常对照组和生理盐水组比较,Aβ1-42组大鼠学习记忆能力下降,大脑皮层和海马部位神经细胞Bcl-2表达量减少,Caspase-3表达量增加（P〈0.01）。与Aβ1-42组比较,二氮嗪＋Aβ1-42组大鼠学习记忆能力有所提高,神经细胞Bcl-2表达量增加,Caspase-3表达量减少（P〈0.05）。结论二氮嗪能提高Aβ1-42组大鼠的学习记忆能力,可能具有抗细胞凋亡的作用。

英文摘要：

Objective To establish Alzheimer disease（AD） models in Wistar rats using β-amyloid1-42（Aβ1-42） and study the effect of diazoxide on the change of apoptotic factors and the ethology of rat AD models.Methods Aβ1-42 was injected into the bilateral ventricles of all the rats,and two weeks later the AD models were established.Diazoxide was injected into some rats at the same time.Y maze electric stimulation was used to evaluate the capability of study and memory of the rats,and protein electrophoresis was used to detect expressions of Bcl-2 and Caspase-3 in the cortical layer and hippocampus of the rats.Results The capability of study and memory decreased expression of Bcl-2 decreased and expression of Caspase-3 increased in the rats injected with Aβ1-42 compared with the normal rats and those injected with NS（P 0.05）.The capability of study and memory increased expression of Bcl-2 increased and expres-sion of Caspase-3 decreased in the rats injected with Aβ1-42 and diazoxide compared with the rats injected with Aβ1-42 a-lone（P 0.05）.Conclusions The AD models were established by the injection of Aβ1-42 into the bilateral ventricles of the rats.Diazoxide can improve the capability of study and memory,increase Bcl-2 expression and decrease Caspase-3 expression.It is likely that diazoxide can resist neurons apoptosis induced by Aβ1-42.