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	Decreasing oxidative stress and neuroinflammation with a multifunctional peptide rescues memory deficits in mice with Alzheimer disease
	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
刊名	FREE RADICAL BIOLOGY AND MEDICINE
	2014-09-01
卷号	74期号:SEP.页码:50-63
关键词	Alzheimer disease beta-Amyloid Oxidative stress Peptide Inflammation Free radicals
ISSN号	0891-5849
其他题名	Free Radic. Biol. Med.
中文摘要	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.
英文摘要	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.
WOS标题词	Science & Technology ; Life Sciences & Biomedicine
类目[WOS]	Biochemistry & Molecular Biology ; Endocrinology & Metabolism
研究领域[WOS]	Biochemistry & Molecular Biology ; Endocrinology & Metabolism
关键词[WOS]	BETA-AMYLOID AGGREGATION ; ANTIBODIES SPECIFICALLY RECOGNIZE ; APPSWE/PS1DE9 MOUSE MODEL ; A-BETA ; NEURODEGENERATIVE DISEASE ; INDUCED NEUROTOXICITY ; PHAGE DISPLAY ; INFLAMMATION ; CYTOTOXICITY ; DYSFUNCTION
收录类别	SCI
原文出处	://WOS:000341274100005
语种	英语
WOS记录号	WOS:000341274100005
公开日期	2014-09-30
内容类型	期刊论文
版本	出版稿
源URL	[http://ir.ipe.ac.cn/handle/122111/11635]
专题	过程工程研究所_研究所（批量导入）
作者单位	1.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
推荐引用方式 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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