Long-term ginsenoside consumption prevents memory loss in aged SAMP8 mice by decreasing oxidative stress and up-regulating the plasticity-related proteins in hippocampus.
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 Abeta 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 Catalyticbeta subunit (p-PKA Cbeta) and protein kinase Cgamma subunit (PKCgamma), 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.
Zhao
Haifeng
H
Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100083, PR China.
Li
Qiong
Q
Zhang
Zhaofeng
Z
Pei
Xinrong
X
Wang
Junbo
J
Li
Yong
Y
D000375:Aging; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects; D016923:Cell Death / Q000187:drug effects; D005106:Exploratory Behavior / Q000187:drug effects; D015870:Gene Expression / Q000187:drug effects; D036145:Ginsenosides / Q000008:administration & dosage*; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018782:Maze Learning / Q000187:drug effects; D008569:Memory Disorders / Q000517:prevention & control*; D051379:Mice; D008822:Mice, Transgenic; D009043:Motor Activity / Q000187:drug effects; D009473:Neuronal Plasticity / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects / Q000648:ultrastructure; D018384:Oxidative Stress / Q000187:drug effects*; D010446:Peptide Fragments / Q000378:metabolism
D016229:Amyloid beta-Peptides; D036145:Ginsenosides; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); D008315:Malondialdehyde