文献类型：期刊文献

英文题名：Chitooligosaccharides protect rat cortical neurons against copper induced damage by attenuating intracellular level of reactive oxygen species

作者：Xu, Wei;Huang, Han-chang;Lin, Chang-jun;Jiang, Zhao-Feng[1]

第一作者：许文

通讯作者：Jiang, ZF[1]

机构：[1]Beijing Union Univ, Coll Arts & Sci, Beijing 100191, Peoples R China; Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, 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, Coll Arts & Sci, Beijing 100191, Peoples R China.|[114172]北京联合大学应用文理学院;[11417]北京联合大学;

年份：2010

卷号：20

期号：10

起止页码：3084-3088

外文期刊名：BIOORGANIC & MEDICINAL CHEMISTRY LETTERS

收录：;Scopus(收录号：2-s2.0-77952105334);WOS:【SCI-EXPANDED(收录号:WOS:000277246300014)】；

基金：This research was supported by Funding Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality (PHR (IHLB)) [PHR20090513].

语种：英文

外文关键词：Copper; Neurotoxicity; COSs; Neuroprotective effects; Oxidative damage; Cortical neurons

摘要：A large number of evidence has suggests that dyshomeostasis of the redox-active biometals such as copper and other metal ions can lead to oxidative stress in neurons, which plays a key role in the pathology of neurodegenerative disorders. Chitooligosaccharides (COSs) are biodegradation product of chitosan and demonstrated diverse biological activities, Here we first report that protective effects of COSs (M. W. 1500, DD. 90%) against Cu(II) induced neurotoxicity in primary cultured rat cortical neurons. The toxicity of Cu(II) to cortical neurons was obviously attenuated in a concentration-dependent manner by COSs pre-treated. The data derived from lactate dehydrogenase (LDH) release and the Hoechst 33342 assay support the results from MTT assay. After DCFH assay, COSs were found to depress Cu(II) induced elevation in intracellular reactive oxygen species (ROS), These findings suggest that COSs protect against Cu(II) induced neurotoxicity in primary cortical neurons by interfering with an increase in intracellular reactive oxygen species (ROS). (C) 2010 Elsevier Ltd. All rights reserved.