Decreasing oxidative stress and neuroinflammation with a multifunctional peptide rescues memory deficits in mice with Alzheimer disease
文献类型：期刊论文
| 作者 | 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
 |
| 出版日期 | 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 | |
| 语种 | 英语 |
| WOS记录号 | WOS:000341274100005 |
| 公开日期 | 2014-09-30 |
| 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. |
入库方式： OAI收割
来源：过程工程研究所
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