Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced by d-Galactose

Adult hippocampal neurogenesis plays a pivotal role in learning and memory. The suppression of hippocampal neurogenesis induced by an increase of oxidative stress is closely related to cognitive impairment. Neural stem cells which persist in the adult vertebrate brain keep up the production of neuro...

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Veröffentlicht in:Neurochemical research 2018-02, Vol.43 (2), p.430-440
Hauptverfasser: Chen, Linbo, Yao, Hui, Chen, Xiongbin, Wang, Ziling, Xiang, Yue, Xia, Jieyu, Liu, Ying, Wang, Yaping
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container_title Neurochemical research
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Yao, Hui
Chen, Xiongbin
Wang, Ziling
Xiang, Yue
Xia, Jieyu
Liu, Ying
Wang, Yaping
description Adult hippocampal neurogenesis plays a pivotal role in learning and memory. The suppression of hippocampal neurogenesis induced by an increase of oxidative stress is closely related to cognitive impairment. Neural stem cells which persist in the adult vertebrate brain keep up the production of neurons over the lifespan. The balance between pro-oxidants and anti-oxidants is important for function and surviving of neural stem cells. Ginsenoside Rg1 is one of the most active components of Panax ginseng, and many studies suggest that ginsenosides have antioxidant properties. This research explored the effects and underlying mechanisms of ginsenoside Rg1 on protecting neural stem cells (NSCs) from oxidative stress. The sub-acute ageing of C57BL/6 mice was induced by subcutaneous injection of d -gal (120 mg kg −1  day −1 ) for 42 day. On the 14th day of d -gal injection, the mice were treated with ginsenoside Rg1 (20 mg kg −1  day −1 , intraperitoneally) or normal saline for 28 days. The study monitored the effects of Rg1 on proliferation, senescence-associated and oxidative stress biomarkers, and Akt/mTOR signalling pathway in NSCs. Compared with the d -gal group, Rg1 improved cognitive impairment induced by d -galactose in mice by attenuating senescence of neural stem cells. Rg1 also decreased the level of oxidative stress, with increased the activity of superoxide dismutase and glutathione peroxidase in vivo and in vitro. Rg1 furthermore reduced the phosphorylation levels of protein kinase B (Akt) and the mechanistic target of rapamycin (mTOR) and down-regulated the levels of downstream p53, p16, p21 and Rb in d -gal treated NSCs. The results suggested that the protective effect of ginsenoside Rg1 on attenuating cognitive impairment in mice and senescence of NSCs induced by d -gal might be related to the reduction of oxidative stress and the down-regulation of Akt/mTOR signaling pathway.
doi_str_mv 10.1007/s11064-017-2438-y
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The suppression of hippocampal neurogenesis induced by an increase of oxidative stress is closely related to cognitive impairment. Neural stem cells which persist in the adult vertebrate brain keep up the production of neurons over the lifespan. The balance between pro-oxidants and anti-oxidants is important for function and surviving of neural stem cells. Ginsenoside Rg1 is one of the most active components of Panax ginseng, and many studies suggest that ginsenosides have antioxidant properties. This research explored the effects and underlying mechanisms of ginsenoside Rg1 on protecting neural stem cells (NSCs) from oxidative stress. The sub-acute ageing of C57BL/6 mice was induced by subcutaneous injection of d -gal (120 mg kg −1  day −1 ) for 42 day. On the 14th day of d -gal injection, the mice were treated with ginsenoside Rg1 (20 mg kg −1  day −1 , intraperitoneally) or normal saline for 28 days. 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The study monitored the effects of Rg1 on proliferation, senescence-associated and oxidative stress biomarkers, and Akt/mTOR signalling pathway in NSCs. Compared with the d -gal group, Rg1 improved cognitive impairment induced by d -galactose in mice by attenuating senescence of neural stem cells. Rg1 also decreased the level of oxidative stress, with increased the activity of superoxide dismutase and glutathione peroxidase in vivo and in vitro. Rg1 furthermore reduced the phosphorylation levels of protein kinase B (Akt) and the mechanistic target of rapamycin (mTOR) and down-regulated the levels of downstream p53, p16, p21 and Rb in d -gal treated NSCs. The results suggested that the protective effect of ginsenoside Rg1 on attenuating cognitive impairment in mice and senescence of NSCs induced by d -gal might be related to the reduction of oxidative stress and the down-regulation of Akt/mTOR signaling pathway.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29147958</pmid><doi>10.1007/s11064-017-2438-y</doi><tpages>11</tpages></addata></record>
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subjects AKT protein
Antioxidants
Attenuation
Biochemistry
Biomarkers
Biomedical and Life Sciences
Biomedicine
Brain
Cell Biology
Cognitive ability
D-Galactose
Galactose
Ginseng
Ginsenosides
Glutathione
Glutathione peroxidase
Hippocampus
Impairment
Injection
Kinases
Learning
Life span
Memory
Mice
Neural stem cells
Neurochemistry
Neurogenesis
Neurology
Neurosciences
Original Paper
Oxidants
Oxidative stress
Oxidizing agents
p53 Protein
Panax ginseng
Peroxidase
Phosphorylation
Rapamycin
Senescence
Signal transduction
Signaling
Stem cells
Superoxide dismutase
title Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced by d-Galactose
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