文献类型：期刊文献

英文题名：Chitosan oligosaccharides alleviate cognitive deficits in an amyloid-beta(1-42)-induced rat model of Alzheimer's disease

作者：Jia, Shiliang[1];Lu, Zheng[1];Gao, Zhaolan[1];An, Jun[1];Wu, Xueling[1];Li, Xiaoxiao[1];Dai, Xueling[1];Zheng, Qiusheng[2];Sun, Yaxuan[1]

第一作者：Jia, Shiliang

通讯作者：Sun, YX[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Binzhou Med Univ, Yantai 264003, Shandong, Peoples R China

第一机构：北京联合大学生物化学工程学院|北京联合大学应用文理学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China.|[1141726]北京联合大学生物化学工程学院;[11417]北京联合大学;[114172]北京联合大学应用文理学院;

年份：2016

卷号：83

起止页码：416-425

外文期刊名：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000369200500049)】；

基金：The authors acknowledge the financial support provided by the Scientific Research Common Program of Beijing Municipal Commission of Education (SQKM201411417014) and the Beijing Union University Campus Project (zk70201402).

语种：英文

外文关键词：Alzheimer's disease; Amyloid-beta(1-42); Chitosan oligosaccharides; Oxidative stress; Neuroinflammation

摘要：Aim: The objective of the present study was two-fold: (i) to evaluate the modulating effects of chitosan oligosaccharides (COS) on cognitive deficits and (ii) to explore their underlying molecular mechanisms. Methods: The Morris water maze and passive avoidance tests were used to determine the neuroprotective effects of COS on A beta(1-42)-induced learning and memory impairments. Biochemical methods were then used to assess COS antioxidant activity in hippocampus, including effects on apoptosis (TUNEL assay) and changes in inflammatory mediators (immunohistochemistry). Results: Orally administered COS at 200, 400, or 800 mg/kg doses were effective at reducing the learning and memory deficits in A beta(1-42)-induced rats. These same doses were also able to ameliorate neuronal apoptosis. The neuroprotective effects of COS were closely associated with its ability to inhibit oxidative stress. This was shown with decreasing levels of malondialdehyde, 8-hydroxy-2'-deoxyguanosine and increasing levels of glutathione peroxidase and super oxide dismutase activities. COS were also shown to suppress the inflammatory response and decrease measures of inflammation via a decrease in the release of proinflammatory cytokines (e.g. interleukin-1beta and tumor necrosis factor-alpha). Conclusion: Taken together, our findings suggest that COS have beneficial effects on the cognitive impairments seen in an A beta(1-42)-induced model of Alzheimer's disease via inhibiting oxidative stress and neuroinflammatory responses. (C) 2015 Elsevier B.V. All rights reserved.