刘贵娟,李卓悦,石杰,等.羧甲基壳寡糖对阿尔茨海默病模型大鼠的作用研究[J].中国海洋药物,2015,34(5):26-32.
羧甲基壳寡糖对阿尔茨海默病模型大鼠的作用研究
Study on the carboxymethyl chitosan oligosaccharide effect of rats models with Alzheimer's disease
投稿时间:2015-03-10  修订日期:2015-04-20
DOI:
中文关键词:  阿尔茨海默氏病  羧甲基壳寡糖  β-淀粉样蛋白
English Keywords:Alzheimer
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作者单位E-mail
刘贵娟 中国海洋大学 海洋生命学院 liuguijuanly@163.com 
李卓悦 中国海洋大学 海洋生命学院  
石杰 中国海洋大学 海洋生命学院  
蒋志雯 中国海洋大学 海洋生命学院  
何明 中国海洋大学 海洋生命学院  
刘万顺 中国海洋大学 海洋生命学院  
韩宝芹* 中国海洋大学 海洋生命学院 baoqinh@ouc.edu.cn 
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中文摘要:
      目的 探讨不同剂量的羧甲基壳寡糖对阿尔茨海默病(Alzheimer's disease,AD)模型大鼠的作用效果及机制。方法 通过侧脑室注射β-淀粉样蛋白(Aβ25-35)建立老年痴呆症大鼠模型,以羧甲基壳寡糖(CM-COS)高剂量(250mg?kg?1?d ?1)和低剂量(150mg?kg?1?d ?1)对模型组大鼠进行连续4周的灌胃治疗,通过Morris水迷宫实验检测大鼠的学习记忆能力,通过测定大鼠海马组织中的MDA、A-CHE、SOD、CHAT及GSH-PX的含量,研究CM-COS对AD大鼠的作用效果及机制。结果 CM-COS高低剂量组均能明显缩短大鼠逃避潜伏期的时间,增加其穿越平台的次数,均能明显降低大鼠大脑海马区MDA和A-CHE的含量,显著提高SOD、CHAT及GSH-PX的含量。结论 CM-COS通过提高AD大鼠海马组织的抗氧化能力和改善其胆碱能系统,从而改善AD大鼠的学习记忆能力,对Aβ25-35所致的老年痴呆症有一定的改善作用。
English Summary:
      Objective To investigate the effect and mechanism of carboxymethyl chitosan oligosaccharide on Alzheimer?s disease model rats. Methods Aβ25-35was injected into the rats lateral ventricle to make AD models. Using the different doses of carboxymethyl chitosan oligosaccharide (CM-COS) respectively,the model group rats were intragastric administration therapy. After intragastric administration for 4 weeks,the learning and memory ability of rats were tested with Morris water labyrinth. To determine the role of CM-COS on the effect and mechanism of AD rat, the content of MDA, A-CHE, SOD, CHAT and GSH-PX in the rats hippocampal tissue were measured. Results CM-COS could significantly decrease the content of MDA and A-CHE in hippocampus of animal models and could significantly increase the content of SOD, CHAT and GSH-PX. Morris water labyrinth experiment results showed that carboxymethyl chitosan oligosaccharide could significantly shorten the animal escape latency time and increase the number of cross platform. Conclusion CM-COS in hippocampal tissue could improvetheability of learning and memory in AD rats by increasing the antioxidant capacity and improving the cholinergic system,and had a certain therapeutic effect on Aβ25-35 caused by Alzheimer's disease.
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