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学科主题: 公共卫生
题名:
Long-term ginsenoside consumption prevents memory loss in aged SAMP8 mice by decreasing oxidative stress and up-regulating the plasticity-related proteins in hippocampus
作者: 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
发表日期: 2009-02-23
DOI: 10.1016/j.brainres.2008.12.031
卷: 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
所属项目编号: 2006BAD27B08
项目资助者: Ministry of Science and Technology of the People&prime ; s Republic of China
WOS记录号: WOS:000264072800013
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/59903
Appears in Collections:北京大学公共卫生学院_期刊论文

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作者单位: Peking Univ, Sch Publ Hlth, Dept Food Hyg & Nutr, Beijing 100083, Peoples R China

Recommended Citation:
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.
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