摘  要:目的：通过体内试验来探讨壳寡糖对利用寡居型Aβ所造模达成的痴呆大鼠动物模型的保护作用。方法：将适应性饲养14天的SD品系大鼠分成3组进行造模，痴呆模型组和壳寡糖灌胃组的造模是通过向大鼠脑双侧海马分别进行脑内注射Aβ来达成，同时设立手术创伤对照组，既向双侧海马注射生理盐水所造的空白对照组模型，保护过程是将壳寡糖溶液以灌胃的方式送入其中一组痴呆模型组的模型大鼠的体内。行为学的检测是通过利用Morris 水迷宫和被动条件回避箱检测经壳寡糖溶液灌胃后的模型动物与其他组别的模型动物的学习行为与认知能力。通过SPSS 17.0软件来分析所得数据间的差异性。并得出结论。结果：Morris水迷宫的结果显示对照组的找到平台的潜伏期明显的要比痴呆模型组的模型动物要低(P<0.05)，而经过壳寡糖灌胃的壳寡糖灌胃组的动物的找到平台的潜伏期要比痴呆模型组模型动物短(P<0.05)。被动条件回避箱结果则显示对照组进入黑箱的潜伏期要比痴呆模型组的长(P<0.05)，而壳寡糖灌胃组的模型动物要比痴呆模型组的潜伏时间长(P<0.05)。结论：通过一系列的行为学实验证实壳寡糖的确有对双侧海马注射Aβ所导致的痴呆动物模型起到了一定的保护作用。

关键词： 阿尔茨海默病；壳寡糖；Morris水迷宫

Abstract:Objective: To investigate the protective effect of chitooligosaccharides to the dementia rat model induced by the widowhood type Aβ by in vivo experiments. Method: Group SD strain rats into three groups after 14 days adaptive feeding. The dementia group and protection group were modeling by bilateral hippocampus injection of Aβ, while establish the surgical trauma control group through bilateral hippocampus injection of saline. The protection process is use chitooligosaccharides solution to gavages into the model rats of one group of dementia group. Behavior detection is through the use of the Morris water maze and passive conditioned reflex box to test the different of the study and recognize level between the protection group and the control group and between the protection group and the dementia group. SPSS 17.0 software is to analyze the differences between the group data. Use this result to draw the conclusions. Results: The results of the Morris water maze shows that latency time before the rats find the platform of the rats in control group is shorter than the dementia group animal models (P<0.05). But in the group which the model animal were gavages the chitooligosaccharides, the latency time before these rats find the platform is also shorter than the dementia group’s rats (P<0.05). Passive conditioned reflex box results show that the latency time before the rat into the black box of control group is longer than the dementia group (P<0.05), while the latency time of protection group model animals are also longer than the dementia group (P<0.05). Conclusion: Through a series behavior experiments confirmed that chitooligosaccharides did actually have some protection effect to the dementia animal model which is induced by bilateral hippocampus injection of Aβ.

Key Words：Alzheimer's disease, chitooligosaccharides, Morris water maze