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Decreasing oxidative stress and neuroinflammation with a multifunctional peptide rescues memory deficits in mice with Alzheimer disease
Alternative TitleFree Radic. Biol. Med.
Zhou, Wei-wei1; Lu, Shuai1; Su, Ya-jing1,2; Xue, Di2; Yu, Xiao-lin1; Wang, Shao-wei1; Zhang, He1; Xu, Peng-xin1,2; Xie, Xi-xiu1; Liu, Rui-tian1
2014-09-01
Source PublicationFREE RADICAL BIOLOGY AND MEDICINE
ISSN0891-5849
Volume74Issue:SEP.Pages:50-63
AbstractAlzheimer disease (AD) is characterized by extracellular senile plaques, intracellular neurofibrillary tangles, and memory loss. Aggregated amyloid-P (A beta), oxidative stress, and inflammation have pivotal roles in the pathogenesis of AD. Therefore, the inhibition of A beta-induced neurotoxicity, oxidative stress, and inflammation is a potential therapeutic strategy for the treatment of AD. In this study, a heptapeptide, isolated from a Ph.D.-C7C library by phage display, attenuated A beta 42-induced cytotoxicity in SH-SY5Y neuroblastoma cells and reduced A beta 42-induced oxidative stress by decreasing the production of reactive oxygen species and glutathione disulfide. As a result, glutathione level increased and superoxide dismutase and glutathione peroxidase activities were enhanced in vitro and in vivo. This peptide also suppressed the inflammatory response by decreasing the release of proinflammatory cytokines, such as tumor necrosis factor alpha and interleukin 1 beta, in microglia and by reducing microgliosis and astrogliosis in AD transgenic mice. This peptide was intracerebroventricularly administered to APPswe/PS1dE9 transgenic mice. We found that this peptide significantly improved spatial memory and reduced the amyloid plaque burden and soluble and insoluble A beta levels. Our findings suggest that this multifunctional peptide has therapeutic potential for an A beta-targeted treatment of AD. (C) 2014 Elsevier Inc. All rights reserved.; Alzheimer disease (AD) is characterized by extracellular senile plaques, intracellular neurofibrillary tangles, and memory loss. Aggregated amyloid-P (A beta), oxidative stress, and inflammation have pivotal roles in the pathogenesis of AD. Therefore, the inhibition of A beta-induced neurotoxicity, oxidative stress, and inflammation is a potential therapeutic strategy for the treatment of AD. In this study, a heptapeptide, isolated from a Ph.D.-C7C library by phage display, attenuated A beta 42-induced cytotoxicity in SH-SY5Y neuroblastoma cells and reduced A beta 42-induced oxidative stress by decreasing the production of reactive oxygen species and glutathione disulfide. As a result, glutathione level increased and superoxide dismutase and glutathione peroxidase activities were enhanced in vitro and in vivo. This peptide also suppressed the inflammatory response by decreasing the release of proinflammatory cytokines, such as tumor necrosis factor alpha and interleukin 1 beta, in microglia and by reducing microgliosis and astrogliosis in AD transgenic mice. This peptide was intracerebroventricularly administered to APPswe/PS1dE9 transgenic mice. We found that this peptide significantly improved spatial memory and reduced the amyloid plaque burden and soluble and insoluble A beta levels. Our findings suggest that this multifunctional peptide has therapeutic potential for an A beta-targeted treatment of AD. (C) 2014 Elsevier Inc. All rights reserved.
KeywordAlzheimer Disease Beta-amyloid Oxidative Stress Peptide Inflammation Free Radicals
SubtypeArticle
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
DOI10.1016/j.freeradbiomed.2014.06.013
URL查看原文
Indexed BySCI
Language英语
WOS KeywordBETA-AMYLOID AGGREGATION ; ANTIBODIES SPECIFICALLY RECOGNIZE ; APPSWE/PS1DE9 MOUSE MODEL ; A-BETA ; NEURODEGENERATIVE DISEASE ; INDUCED NEUROTOXICITY ; PHAGE DISPLAY ; INFLAMMATION ; CYTOTOXICITY ; DYSFUNCTION
WOS Research AreaBiochemistry & Molecular Biology ; Endocrinology & Metabolism
WOS SubjectBiochemistry & Molecular Biology ; Endocrinology & Metabolism
WOS IDWOS:000341274100005
Citation statistics
Cited Times:34[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Version出版稿
Identifierhttp://ir.ipe.ac.cn/handle/122111/11635
Collection研究所(批量导入)
Affiliation1.Chinese Acad Sci, Inst Proc Engn, Natl Key Lab Biochem Engn, Beijing 100190, Peoples R China
2.Ningxia Univ, Sch Life Sci, Yinchuan 750021, Peoples R China
Recommended Citation
GB/T 7714
Zhou, Wei-wei,Lu, Shuai,Su, Ya-jing,et al. Decreasing oxidative stress and neuroinflammation with a multifunctional peptide rescues memory deficits in mice with Alzheimer disease[J]. FREE RADICAL BIOLOGY AND MEDICINE,2014,74(SEP.):50-63.
APA Zhou, Wei-wei.,Lu, Shuai.,Su, Ya-jing.,Xue, Di.,Yu, Xiao-lin.,...&Liu, Rui-tian.(2014).Decreasing oxidative stress and neuroinflammation with a multifunctional peptide rescues memory deficits in mice with Alzheimer disease.FREE RADICAL BIOLOGY AND MEDICINE,74(SEP.),50-63.
MLA Zhou, Wei-wei,et al."Decreasing oxidative stress and neuroinflammation with a multifunctional peptide rescues memory deficits in mice with Alzheimer disease".FREE RADICAL BIOLOGY AND MEDICINE 74.SEP.(2014):50-63.
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