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。
Objective To investigate the effect and mechanism of carboxymethyl chitosan oligosaccharide on Alzheimers disease model rats. Methods Aβ25-35was injected into the rats lateral ventricle to maike AD models. Using the different doses of carboxymethy[ chitosan oiigosaccharide （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 in- crease 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 im- provetheability of learning and memory in AD rats by increasing the antioxidant capacity and improvingthe cholinergic system,and had a certain therapeutic effect on A1325 35 caused by Alzheimer＇s disease.
出处
《中国海洋药物》
CAS
CSCD
2015年第5期26-32,共7页
Chinese Journal of Marine Drugs
基金
国家"十二五"科技支撑计划课题(2013BAB01B02)资助
关键词
阿尔茨海默氏病
羧甲基壳寡糖
Β-淀粉样蛋白
Alzheimefs disease
carboxymethyl chitosan oligosaccharide
amyloid beta protein
