Long-term ginsenoside administration prevents memory impairment in aged C57BL/6J mice by up-regulating the synaptic plasticity-related proteins in hippocampus.
Memory impairment is considered to be one of the most prominent consequences of aging. Deterioration of memory begins in advance of old age in animals, including humans. Thus, it is extremely important to prevent memory decline for increasing healthy aging. Ginsenoside, the effective ingredient of ginseng, has been reported to have a neuron beneficial effect, but the preventive role on memory impairment and the underlying mechanisms have not been well determined. In the present study, C57BL/6J mice aged 12 months were chronically treated with ginsenoside 100mg/kg per day for 8 months. Placebo-treated aged mice, young and adult ones (4- and 8-month-old, respectively) were used as controls. The efficacious effect of ginsenoside was manifested in the amelioration of memory impairment in aged mice by Morris water maze and step-down tests. Compared with aged control group, the plasticity-related proteins including phospho-N-methyl-d-aspartate receptor1 (NMDAR1), phospho-calcium-calmodulin dependent kinase II (CaMK II), phospho-PKA catalytic beta subunit (PKA Cbeta), phospho-cAMP-response element binding protein (CREB) and brain derived neurotrophic factor (BDNF) in hippocampus significantly increased in ginsenoside treated group. These findings suggest that ginsenoside is effective on the prevention of age-related memory impairment, and the up-regulation of plasticity-related proteins in hippocampus may be one of the mechanisms.
Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Xueyuan Road 38, Beijing 100191, PR China.
Haifeng
H
Zhao
Qiong
Q
Li
Xinrong
X
Pei
Zhaofeng
Z
Zhang
Ruiyue
R
Yang
Junbo
J
Wang
Yong
Y
Li
D000375:Aging / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology; D019208:Brain-Derived Neurotrophic Factor / Q000187:drug effects / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000187:drug effects / Q000378:metabolism; D017362:Cyclic AMP Response Element-Binding Protein / Q000187:drug effects / Q000378:metabolism; D054751:Cyclic AMP-Dependent Protein Kinase Catalytic Subunits / Q000187:drug effects / Q000378:metabolism; D005260:Female; D036145:Ginsenosides / Q000008:administration & dosage*; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology*; D018782:Maze Learning / Q000187:drug effects* / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D009419:Nerve Tissue Proteins / Q000187:drug effects / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology; D018697:Nootropic Agents / Q000008:administration & dosage*; D011597:Psychomotor Performance / Q000187:drug effects / Q000502:physiology; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors
D019208:Brain-Derived Neurotrophic Factor; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017362:Cyclic AMP Response Element-Binding Protein; D054751:Cyclic AMP-Dependent Protein Kinase Catalytic Subunits; D036145:Ginsenosides; D009419:Nerve Tissue Proteins; D018697:Nootropic Agents; D016194:Receptors, N-Methyl-D-Aspartate