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Long-term ginsenoside consumption prevents memory loss in aged SAMP8 mice by decreasing oxidative stress and up-regulating the plasticity-related proteins in hippocampus
Zhao, Haifeng; Li, Qiong; Zhang, Zhaofeng; Pei, Xinrong; Wang, Junbo; Li, Yong
关键词Ginsenoside Memory SAMP8 mice Oxidative stress Plasticity
刊名BRAIN RESEARCH
2009-02-23
DOI10.1016/j.brainres.2008.12.031
1256页:111-122
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]SENESCENCE-ACCELERATED MICE ; SYNAPTIC PLASTICITY ; ALZHEIMERS-DISEASE ; GENE-EXPRESSION ; NMDAR1 SUBUNIT ; MURINE MODEL ; AGING BRAIN ; KINASE-II ; MOUSE SAM ; LIFE-SPAN
英文摘要

Ginsenoside, the effective component of ginseng, has been reported to have a neuron protective effect, but the preventive effect on Alzheimer′s disease (AD) related memory loss and the underlying mechanisms have not been well determined. The senescence-accelerated mouse (SAM) is a useful model of AD-related memory impairment. In the present study, SAMP8 mice aged 4 months were chronically treated with ginsenoside (3 dose groups were given ginsenoside in drinking water for 7 months). The three groups were treated with ginsenoside 50, 100 and 200 mg/kg per day, respectively. Placebo-treated aged mice and young ones (4 months old) were used as controls. In addition, SAMR1 mice were used as "normal aging" control. The beneficial role of ginsenoside was manifested in the prevention of memory loss in aged SAMP8 mice. The optimal dose of ginsenoside is 100 or 200 mg/kg per day. In ginsenoside treated groups, the A beta level markedly decreased in hippocampus and antioxidase level significantly increased in serum. In addition, the plasticity-related proteins in hippocampus significantly increased in the two ginsenoside treated groups. The plasticity-related proteins were checked in the present study including postsynaptic density-95 (PSD-95), phosphor-N-methyl-D-aspartate receptor 1 (p-NMDAR1), phospho-calcium-calmodulin dependent kinase II (p-CaMKII), phospho-protein kinase A Catalytic beta subunit (p-PKA C beta) and protein kinase C gamma subunit (PKC gamma), phospho-CREB (p-CREB) and brain derived neurotrophic factor (BDNF) etc. These findings suggest that the increase of antioxidation and up-regulation of plasticity-related proteins in hippocampus may be one of the mechanisms of ginsenoside on the memory loss prevention in aged SAMP8 mice. (C) 2008 Elsevier B.V. All rights reserved.

语种英语
WOS记录号WOS:000264072800013
引用统计
被引频次:63[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/400002259/59903
专题北京大学公共卫生学院
北京大学公共卫生学院_营养与食品卫生学系
北京大学公共卫生学院_公共卫生学院
作者单位Peking Univ, Sch Publ Hlth, Dept Food Hyg & Nutr, Beijing 100083, Peoples R China
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GB/T 7714
Zhao, Haifeng,Li, Qiong,Zhang, Zhaofeng,et al. Long-term ginsenoside consumption prevents memory loss in aged SAMP8 mice by decreasing oxidative stress and up-regulating the plasticity-related proteins in hippocampus[J]. BRAIN RESEARCH,2009,1256:111-122.
APA Zhao, Haifeng,Li, Qiong,Zhang, Zhaofeng,Pei, Xinrong,Wang, Junbo,&Li, Yong.(2009).Long-term ginsenoside consumption prevents memory loss in aged SAMP8 mice by decreasing oxidative stress and up-regulating the plasticity-related proteins in hippocampus.BRAIN RESEARCH,1256,111-122.
MLA Zhao, Haifeng,et al."Long-term ginsenoside consumption prevents memory loss in aged SAMP8 mice by decreasing oxidative stress and up-regulating the plasticity-related proteins in hippocampus".BRAIN RESEARCH 1256(2009):111-122.
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