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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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 |
format | Article |
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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.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-017-2438-y</identifier><identifier>PMID: 29147958</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>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</subject><ispartof>Neurochemical research, 2018-02, Vol.43 (2), p.430-440</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2017</rights><rights>Neurochemical Research is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-3317eec11630a9389a59e4926cd5211eb5d9e44da0af6f2591ae7e904bed92193</citedby><cites>FETCH-LOGICAL-c372t-3317eec11630a9389a59e4926cd5211eb5d9e44da0af6f2591ae7e904bed92193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-017-2438-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-017-2438-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29147958$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Linbo</creatorcontrib><creatorcontrib>Yao, Hui</creatorcontrib><creatorcontrib>Chen, Xiongbin</creatorcontrib><creatorcontrib>Wang, Ziling</creatorcontrib><creatorcontrib>Xiang, Yue</creatorcontrib><creatorcontrib>Xia, Jieyu</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Wang, Yaping</creatorcontrib><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</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><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.</description><subject>AKT protein</subject><subject>Antioxidants</subject><subject>Attenuation</subject><subject>Biochemistry</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Cell Biology</subject><subject>Cognitive ability</subject><subject>D-Galactose</subject><subject>Galactose</subject><subject>Ginseng</subject><subject>Ginsenosides</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Hippocampus</subject><subject>Impairment</subject><subject>Injection</subject><subject>Kinases</subject><subject>Learning</subject><subject>Life span</subject><subject>Memory</subject><subject>Mice</subject><subject>Neural stem cells</subject><subject>Neurochemistry</subject><subject>Neurogenesis</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Oxidants</subject><subject>Oxidative stress</subject><subject>Oxidizing agents</subject><subject>p53 Protein</subject><subject>Panax ginseng</subject><subject>Peroxidase</subject><subject>Phosphorylation</subject><subject>Rapamycin</subject><subject>Senescence</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Stem cells</subject><subject>Superoxide dismutase</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp1kc9uEzEQxi0EoqHwAFyQJS5clnrs_edjlNIQqRApKeeVs55duezawfZC82I8H05SEELiNBrN7_tmNB8hr4G9B8aqqwDAyjxjUGU8F3V2eEJmUFQiKyUTT8mMiTQVINkFeRHCPWNJxeE5ueAS8koW9Yz8XBob0LpgNNJND_QaW48qYKDrB6NVNN-RbqPHEKiyml67HzbbYD8NKiZm_jVejXfrDd2a3qphMLan0dF5jGinRNCF6605mazGvTJ-RBupsfSTafFkuEWLoUWbWtfRzzh5NaSFONIFDkOgK6unFjXdHajOlmpQbXQBX5JnnRoCvnqsl-TLzYe7xcfsdr1cLea3WSsqHjMhoEJsAUrBlBS1VIXEXPKy1QUHwF2hU59rxVRXdryQoLBCyfIdaslBikvy7uy79-7bhCE2o0nXDoOy6KbQgCxLnud1cUTf_oPeu8mnp5yoogBZ1Xmi4Ey13oXgsWv23ozKHxpgzTHU5hxqk0JtjqE2h6R58-g87UbUfxS_U0wAPwMhjWyP_q_V_3X9BTx5rmo</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Chen, Linbo</creator><creator>Yao, Hui</creator><creator>Chen, Xiongbin</creator><creator>Wang, Ziling</creator><creator>Xiang, Yue</creator><creator>Xia, Jieyu</creator><creator>Liu, Ying</creator><creator>Wang, Yaping</creator><general>Springer US</general><general>Springer Nature 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in Mice and Senescence of Neural Stem Cells Induced by d-Galactose</title><author>Chen, Linbo ; Yao, Hui ; Chen, Xiongbin ; Wang, Ziling ; Xiang, Yue ; Xia, Jieyu ; Liu, Ying ; Wang, Yaping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-3317eec11630a9389a59e4926cd5211eb5d9e44da0af6f2591ae7e904bed92193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>AKT protein</topic><topic>Antioxidants</topic><topic>Attenuation</topic><topic>Biochemistry</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Cell Biology</topic><topic>Cognitive ability</topic><topic>D-Galactose</topic><topic>Galactose</topic><topic>Ginseng</topic><topic>Ginsenosides</topic><topic>Glutathione</topic><topic>Glutathione peroxidase</topic><topic>Hippocampus</topic><topic>Impairment</topic><topic>Injection</topic><topic>Kinases</topic><topic>Learning</topic><topic>Life span</topic><topic>Memory</topic><topic>Mice</topic><topic>Neural stem cells</topic><topic>Neurochemistry</topic><topic>Neurogenesis</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Oxidants</topic><topic>Oxidative stress</topic><topic>Oxidizing agents</topic><topic>p53 Protein</topic><topic>Panax ginseng</topic><topic>Peroxidase</topic><topic>Phosphorylation</topic><topic>Rapamycin</topic><topic>Senescence</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Stem cells</topic><topic>Superoxide dismutase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Linbo</creatorcontrib><creatorcontrib>Yao, Hui</creatorcontrib><creatorcontrib>Chen, Xiongbin</creatorcontrib><creatorcontrib>Wang, Ziling</creatorcontrib><creatorcontrib>Xiang, Yue</creatorcontrib><creatorcontrib>Xia, Jieyu</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Wang, Yaping</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection 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Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced by d-Galactose</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>43</volume><issue>2</issue><spage>430</spage><epage>440</epage><pages>430-440</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>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.</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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