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Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric beta-amyloid 1-42-induced neurotoxicity
Dai, Xueling1,2,3; Chang, Ping1,3; Zhu, Qingzhu1; Liu, Wenjuan1,3; Sun, Yaxuan1; Zhu, Shigong2; Jiang, Zhaofeng1,3
关键词Alzheimer&prime s disease beta-Amyloid peptide Chitosan oligosaccharides Neurotoxicity
刊名NEUROSCIENCE LETTERS
2013-10-25
DOI10.1016/j.neulet.2013.08.046
554页:64-69
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
资助者NSFC ; Scientific Research Common Program of Beijing Municipal Commission of Education ; NSFC ; Scientific Research Common Program of Beijing Municipal Commission of Education
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]ALZHEIMERS-DISEASE ; OXIDATIVE STRESS ; APOPTOSIS ; CELLS ; INHIBITION ; PEPTIDE ; MICE ; ACTIVATION ; CASPASES ; PATHWAY
英文摘要

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.

语种英语
所属项目编号31071512 ; SQKM 201211417013
资助者NSFC ; Scientific Research Common Program of Beijing Municipal Commission of Education ; NSFC ; Scientific Research Common Program of Beijing Municipal Commission of Education
WOS记录号WOS:000327674600013
引用统计
被引频次:15[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/65404
专题基础医学院
作者单位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
推荐引用方式
GB/T 7714
Dai, Xueling,Chang, Ping,Zhu, Qingzhu,et al. Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric beta-amyloid 1-42-induced neurotoxicity[J]. NEUROSCIENCE LETTERS,2013,554:64-69.
APA Dai, Xueling.,Chang, Ping.,Zhu, Qingzhu.,Liu, Wenjuan.,Sun, Yaxuan.,...&Jiang, Zhaofeng.(2013).Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric beta-amyloid 1-42-induced neurotoxicity.NEUROSCIENCE LETTERS,554,64-69.
MLA Dai, Xueling,et al."Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric beta-amyloid 1-42-induced neurotoxicity".NEUROSCIENCE LETTERS 554(2013):64-69.
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