文献类型：期刊文献

英文题名：Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric beta-amyloid 1-42-induced neurotoxicity

作者：Dai, Xueling[1,2,3];Chang, Ping[1,3];Zhu, Qingzhu[1];Liu, Wenjuan[1,3];Sun, Yaxuan[1];Zhu, Shigong[2];Jiang, Zhaofeng[1,3]

第一作者：Dai, Xueling;戴雪伶

通讯作者：Zhu, SG[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Peking Univ, Sch Basic Med Sci, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China;[3]Beijing Union Univ, Res Inst Sci & Technol Funct Food, Beijing 100191, Peoples R 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]corresponding author), Peking Univ, Sch Basic Med Sci, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China.

年份：2013

卷号：554

起止页码：64-69

外文期刊名：NEUROSCIENCE LETTERS

收录：;Scopus(收录号：2-s2.0-84884385432);WOS:【SCI-EXPANDED(收录号:WOS:000327674600013)】；

基金：This work was supported by grants from NSFC Project 31071512, and grants from Scientific Research Common Program of Beijing Municipal Commission of Education (SQKM 201211417013).

语种：英文

外文关键词：Alzheimer's disease; beta-Amyloid peptide; Chitosan oligosaccharides; Neurotoxicity

摘要：beta-Amyloid peptide (A beta), the major component of senile plaques in patients with Alzheimer's disease (AD), is believed to facilitate the progressive neurodegeneration that occurs in this disease. Mounting natural compounds are proved to be potential candidates for the prevention and treatment of AD. Chitosan oligosaccharides (COSs), the enzymatic hydrolysates of chitosan, have been reported to possess diverse biological activities. Here we investigated the effect of COSs on oligomeric A beta-mediated toxicity in rat primary hippocampal neurons. Pretreatment with COSs markedly inhibited cell death induced by A beta exposure as determined by cell viability assay and lactate dehydrogenase release assay. In parallel, the generation of reactive oxygen species and lipid peroxidation were attenuated by COSs. Furthermore, our results indicated that COSs remarkably prevented A beta-induced cell apoptosis as manifested by depressing the elevation of Bax/Bcl-2 ratio and caspase-3 activation, suggesting that the neuroprotective effect of COSs could be partially due to apoptosis regulation. In addition, pretreatment with COSs significantly blocked A beta-induced phosphorylation of c-Jun N-terminal kinase. Taken together, these findings may shed light on the role of COSs as a potential therapeutic agent for AD. (C) 2013 Elsevier Ireland Ltd. All rights reserved.