文献类型：期刊文献

英文题名：Chitosan oligosaccharides alleviate cognitive deficits in an amyloid-β1-42-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

机构：[1] Beijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing, 100191, China; [2] Binzhou Medical University, Yantai, Shandong, 264003, China

第一机构：北京联合大学应用文理学院|北京联合大学生物化学工程学院

通讯机构：[1]Beijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing, 100191, China|[114172]北京联合大学应用文理学院;[11417]北京联合大学;[1141726]北京联合大学生物化学工程学院;

年份：2016

卷号：83

起止页码：416-425

外文期刊名：International Journal of Biological Macromolecules

收录：EI(收录号：20242616460595);Scopus(收录号：2-s2.0-84953635985)

语种：英文

外文关键词：Chitosan - Glycoproteins - Neurodegenerative diseases - Oligosaccharides - Oxidative stress

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 Aβ1-42-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 800mg/kg doses were effective at reducing the learning and memory deficits in Aβ1-42-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 Aβ1-42-induced model of Alzheimer's disease via inhibiting oxidative stress and neuroinflammatory responses. ? 2015 Elsevier B.V.