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Article: Astragaloside VI Promotes Neural Stem Cell Proliferation and Enhances Neurological Function Recovery in Transient Cerebral Ischemic Injury via Activating EGFR/MAPK Signaling Cascades

TitleAstragaloside VI Promotes Neural Stem Cell Proliferation and Enhances Neurological Function Recovery in Transient Cerebral Ischemic Injury via Activating EGFR/MAPK Signaling Cascades
Authors
Issue Date2019
PublisherHumana Press, Inc. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035
Citation
Molecular Neurobiology, 2019, v. 56 n. 4, p. 3053–3067 How to Cite?
AbstractRadix Astragali (AR) is a commonly used medicinal herb for post-stroke disability in Traditional Chinese Medicine but its active compounds for promoting neurogenic effects are largely unknown. In the present study, we tested the hypothesis that Astragaloside VI could be a promising active compound from AR for adult neurogenesis and brain repair via targeting epidermal growth factor (EGF)-mediated MAPK signaling pathway in post-stroke treatment. By using cultured neural stem cells (NSCs) and experimental stroke rat model, we investigated the effects of Astragaloside VI on inducing NSCs proliferation and self-renewal in vitro, and enhancing neurogenesis for the recovery of the neurological functions in post-ischemic brains in vivo. For animal experiments, rats were undergone 1.5 h middle cerebral artery occlusion (MCAO) plus 7 days reperfusion. Astragaloside VI (2 μg/kg) was daily administrated by intravenous injection (i.v.) for 7 days. Astragaloside VI treatment promoted neurogenesis and astrogenic formation in dentate gyrus zone, subventricular zone, and cortex of the transient ischemic rat brains in vivo. Astragaloside VI treatment enhanced NSCs self-renewal and proliferation in the cultured NSCs in vitro without affecting NSCs differentiation. Western blot analysis showed that Astragaloside VI up-regulated the expression of nestin, p-EGFR and p-MAPK, and increased neurosphere sizes, whose effects were abolished by the co-treatment of EGF receptor inhibitor gefitinib and ERK inhibitor PD98059. Behavior tests revealed that Astragaloside VI promoted the spatial learning and memory and improved the impaired motor function in transient cerebral ischemic rats. Taken together, Astragaloside VI could effectively activate EGFR/MAPK signaling cascades, promote NSCs proliferation and neurogenesis in transient cerebral ischemic brains, and improve the repair of neurological functions in post-ischemic stroke rats. Astragaloside VI could be a new therapeutic drug candidate for post-stroke treatment.
Persistent Identifierhttp://hdl.handle.net/10722/259986
ISSN
2017 Impact Factor: 5.076
2015 SCImago Journal Rankings: 1.819

 

DC FieldValueLanguage
dc.contributor.authorChen, X-
dc.contributor.authorWu, H-
dc.contributor.authorChen, H-
dc.contributor.authorWang, Q-
dc.contributor.authorXie, X-
dc.contributor.authorShen, J-
dc.date.accessioned2018-09-03T04:22:26Z-
dc.date.available2018-09-03T04:22:26Z-
dc.date.issued2019-
dc.identifier.citationMolecular Neurobiology, 2019, v. 56 n. 4, p. 3053–3067-
dc.identifier.issn0893-7648-
dc.identifier.urihttp://hdl.handle.net/10722/259986-
dc.description.abstractRadix Astragali (AR) is a commonly used medicinal herb for post-stroke disability in Traditional Chinese Medicine but its active compounds for promoting neurogenic effects are largely unknown. In the present study, we tested the hypothesis that Astragaloside VI could be a promising active compound from AR for adult neurogenesis and brain repair via targeting epidermal growth factor (EGF)-mediated MAPK signaling pathway in post-stroke treatment. By using cultured neural stem cells (NSCs) and experimental stroke rat model, we investigated the effects of Astragaloside VI on inducing NSCs proliferation and self-renewal in vitro, and enhancing neurogenesis for the recovery of the neurological functions in post-ischemic brains in vivo. For animal experiments, rats were undergone 1.5 h middle cerebral artery occlusion (MCAO) plus 7 days reperfusion. Astragaloside VI (2 μg/kg) was daily administrated by intravenous injection (i.v.) for 7 days. Astragaloside VI treatment promoted neurogenesis and astrogenic formation in dentate gyrus zone, subventricular zone, and cortex of the transient ischemic rat brains in vivo. Astragaloside VI treatment enhanced NSCs self-renewal and proliferation in the cultured NSCs in vitro without affecting NSCs differentiation. Western blot analysis showed that Astragaloside VI up-regulated the expression of nestin, p-EGFR and p-MAPK, and increased neurosphere sizes, whose effects were abolished by the co-treatment of EGF receptor inhibitor gefitinib and ERK inhibitor PD98059. Behavior tests revealed that Astragaloside VI promoted the spatial learning and memory and improved the impaired motor function in transient cerebral ischemic rats. Taken together, Astragaloside VI could effectively activate EGFR/MAPK signaling cascades, promote NSCs proliferation and neurogenesis in transient cerebral ischemic brains, and improve the repair of neurological functions in post-ischemic stroke rats. Astragaloside VI could be a new therapeutic drug candidate for post-stroke treatment.-
dc.languageeng-
dc.publisherHumana Press, Inc. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035-
dc.relation.ispartofMolecular Neurobiology-
dc.rightsThis is a post-peer-review, pre-copyedit version of an article published in Molecular Neurobiology. The final authenticated version is available online at: http://dx.doi.org/10.1007/s12035-018-1294-3-
dc.titleAstragaloside VI Promotes Neural Stem Cell Proliferation and Enhances Neurological Function Recovery in Transient Cerebral Ischemic Injury via Activating EGFR/MAPK Signaling Cascades-
dc.typeArticle-
dc.identifier.emailChen, H: chenhs@hku.hk-
dc.identifier.emailShen, J: shenjg@hku.hk-
dc.identifier.authorityShen, J=rp00487-
dc.description.naturepostprint-
dc.identifier.doi10.1007/s12035-018-1294-3-
dc.identifier.hkuros287934-
dc.identifier.volume56-
dc.identifier.issue4-
dc.identifier.spage3053-
dc.identifier.epage3067-
dc.publisher.placeUnited States-

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