壳寡糖对Amyloid-β_(1-42)致痴呆大鼠的学习记忆及血清抗氧化功能的影响

Effect of Chitosan Oligosaccharide on Learning and Memory Functions and Serum Antioxidant Status in a Rat Model of Amyloid-β_(1–42)-Induced Alzheimer's Disease

目的:探讨壳寡糖(chitosan oligosaccharide,COS)对Aβ_(1-42)致痴呆大鼠学习记忆及血清抗氧化功能的影响及其作用机制。方法:采用海马区微注射Aβ_(1-42)建立阿尔茨海默病大鼠痴呆模型,并使用COS干预,通过Morris水迷宫实验观察COS对阿尔茨海默病大鼠学习记忆能力的影响,同时通过测定血清中谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)和超氧化物歧化酶(superoxide dismutase,SOD)等抗氧化酶的活力以及蛋白质羰基和丙二醛(malondialdehyde,MDA)含量变化观察COS的抗氧化能力。结果:经行为学测试,与假手术对照组相比,模型组大鼠的学习记忆能力明显下降;COS干预后,其学习记忆功能力有所改善。同时,模型组大鼠血清中的SOD和GSH-Px活力相比较假手术组显著降低,MDA和蛋白质羰基含量显著增加;经COS干预后,与模型组相比,大鼠血清中SOD和GSH-Px活力显著上升,MDA和蛋白质羰基含量均显著减少。结论:COS对海马区微注射Aβ_(1-42)致痴呆大鼠有一定的改善和保护作用,具体的作用机制可能与COS的抗氧化作用有关。

Aim: The objective of the present study was to evaluate the protective effect of chitosan oligosaccharides (COS) against cognitive deficits and oxidative damage induced by bilateral intrahippocampal (IH) injections of aggreg atedamyloid-β1-42 (Aβ1–42) and to explore the underlying molecular mechanisms. Methods: Morris water maze test was performed to observe the effect of COS on learning and memory in Alzheimer’s disease rats. At the same time, serum super oxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, and protein carbonyl and malondialdehyde (MDA)contents were measured to evaluate the antioxidant capacity of COS. Results: Compared with the sham operation controlgroup, Aβ1–42-exposed rats showed remarkable memory impairment in ethological experiments. In contrast, compared withthe model group, the learning and memory functions of the COS-treated patients were improved. Besides, the rats in themodel group showed significantly lower serum activities of SOD and GSH-Px as well as significantly higher MDA andprotein carbonyl contents compared with the sham operation group. After the intervention of COS, the activities of SOD andGSH-Px significantly were increased, and MDA and protein carbonyl contents were reduced significantly compared with the model group. Conclusion: COS has potential therapeutic effect on Aβ1-42-induced cognitive impairment via inhibiting oxidative stress.