2009Acta Nutrimenta SinicaRequires access

Ginsenoside facilitates learning and memory in aged mice.

Dong Li, Haifeng Hou

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Abstract

Objective To investigate the effect of ginsenoside on degeneration of learning and memory in aged mice and the mechanism. Method Eighty female C57BL/6J mice aged 20-mo were randomly divided into control group and three ginsenoside treatment groups at dosage of 25,50,100 mg/(kg bw·d) respectively by drinking. In addition, 20 female C57BL/6J mice aged 3 mo were used to be young control group. Eight mo later, the learning and memory abilities of the mice were checked by Morris water maze. Thereafter, the mice were killed by decapitation,and their serum was collected to determine the level of SOD, GSH-Px and MDA. Hippocampal morphology was examined by Nissl stain; and the expression of brain-derived neurotrophic factor (BDNF) in hippocampus was studied using Western blot method. Results 50,100 mg/(kg bw·d) ginsenosides administration could significantly shorten the escape latency of the aged mice in Morris water maze. Furthermore,the alleviated oxidative stress and up-regulated expression of BDNF were observed in 50, 100 (mg/kg·d) ginsenosides groups compared with aged control group. Serum level of GSH-Px was higher in 25 (mg/kg bw·d) ginsenosides group compared to that of aged control group. The number of Nissl-positive cell had no significant difference between all groups. Conclusion 50,100 mg/(kg bw·d) ginsenoside can significantly delay the degeneration of learning and memory in aged mice by lowering oxidative damage and up-regulating BDNF expression in hippocampus.

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Objective To investigate the effect of ginsenoside on degeneration of learning and memory in aged mice and the mechanism. Method Eighty female C57BL/6J mice aged 20-mo were randomly divided into control group and three ginsenoside treatment groups at dosage of 25,50,100 mg/(kg bw·d) respectively by drinking. In addition, 20 female C57BL/6J mice aged 3 mo were used to be young control group. Eight mo later, the learning and memory abilities of the mice were checked by Morris water maze. Thereafter, the mice were killed by decapitation,and their serum was collected to determine the level of SOD, GSH-Px and MDA. Hippocampal morphology was examined by Nissl stain; and the expression of brain-derived neurotrophic factor (BDNF) in hippocampus was studied using Western blot method. Results 50,100 mg/(kg bw·d) ginsenosides administration could significantly shorten the escape latency of the aged mice in Morris water maze. Furthermore,the alleviated oxidative stress and up-regulated expression of BDNF were observed in 50, 100 (mg/kg·d) ginsenosides groups compared with aged control group. Serum level of GSH-Px was higher in 25 (mg/kg bw·d) ginsenosides group compared to that of aged control group. The number of Nissl-positive cell had no significant difference between all groups. Conclusion 50,100 mg/(kg bw·d) ginsenoside can significantly delay the degeneration of learning and memory in aged mice by lowering oxidative damage and up-regulating BDNF expression in hippocampus.

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Available abstract

Objective To investigate the effect of ginsenoside on degeneration of learning and memory in aged mice and the mechanism. Method Eighty female C57BL/6J mice aged 20-mo were randomly divided into control group and three ginsenoside treatment groups at dosage of 25,50,100 mg/(kg bw·d) respectively by drinking. In addition, 20 female C57BL/6J mice aged 3 mo were used to be young control group. Eight mo later, the learning and memory abilities of the mice were checked by Morris water maze. Thereafter, the mice were killed by decapitation,and their serum was collected to determine the level of SOD, GSH-Px and MDA. Hippocampal morphology was examined by Nissl stain; and the expression of brain-derived neurotrophic factor (BDNF) in hippocampus was studied using Western blot method. Results 50,100 mg/(kg bw·d) ginsenosides administration could significantly shorten the escape latency of the aged mice in Morris water maze. Furthermore,the alleviated oxidative stress and up-regulated expression of BDNF were observed in 50, 100 (mg/kg·d) ginsenosides groups compared with aged control group. Serum level of GSH-Px was higher in 25 (mg/kg bw·d) ginsenosides group compared to that of aged control group. The number of Nissl-positive cell had no significant difference between all groups. Conclusion 50,100 mg/(kg bw·d) ginsenoside can significantly delay the degeneration of learning and memory in aged mice by lowering oxidative damage and up-regulating BDNF expression in hippocampus.

Key concepts: Nissl body, Morris water navigation task, Hippocampus, Endocrinology, Oxidative stress, Internal medicine, Hippocampal formation, Neurotrophic factors

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