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Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model
BACKGROUND: Ischemic cerebrovascular disease leads to the activation and differentiation of neural stem cells (NSCs) into mature neurons and glia cells to repair nerve damage. Astragalus flavone (ASF) has shown its potential role in proliferation and differentiation into dopamine neurons of NSCs. MA...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8915658/ https://www.ncbi.nlm.nih.gov/pubmed/35250022 http://dx.doi.org/10.12659/MSM.933830 |
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author | Gao, Han Huang, Ningjing Wang, Weiwei Zhang, Lingling Cai, Li Chen, Min Li, Wentao |
author_facet | Gao, Han Huang, Ningjing Wang, Weiwei Zhang, Lingling Cai, Li Chen, Min Li, Wentao |
author_sort | Gao, Han |
collection | PubMed |
description | BACKGROUND: Ischemic cerebrovascular disease leads to the activation and differentiation of neural stem cells (NSCs) into mature neurons and glia cells to repair nerve damage. Astragalus flavone (ASF) has shown its potential role in proliferation and differentiation into dopamine neurons of NSCs. MATERIAL/METHODS: Cerebral infarction models were constructed to determine the effects of ASF on NSCs in vivo and in vitro. RESULTS: ASF therapy had the ability to reduce the neurologic function scores and the cerebral infarction volume of the cerebral infarction model. Moreover, ASF was able to increase BrdU-positive cells and promote the expression of Nestin, β-Tubulin III, and O4, while decreasing the expression of GFAP. qRT-PCR and western blot assays showed ASF promoted the expression of Mash1, Math1, and Ngn2 mRNA and protein in cerebral infarction rats. Meanwhile, ASF (20 μg/ml) was able to increase EdU-positive cells and promote the expression of Nestin, β-Tubulin III, and O4 of NSCs at day14 in vitro. In normoxia, ASF obviously promoted the expression of Mash1, Ngn1, and Ngn2 mRNA and proteins, but in hypoxia, ASF promoted the expression of Notch1 and Math1 mRNA and proteins and inhibited the expression of Ngn1 and Ngn2 mRNA and proteins. CONCLUSIONS: ASF therapy can improve the neurologic functions and reduce the cerebral infarction volume in a cerebral infarction model. Moreover, ASF promoted the proliferation of NSCs and induced differentiation into neurons and oligodendrocytes, which might be involved in regulating factors in Notch signaling. |
format | Online Article Text |
id | pubmed-8915658 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-89156582022-03-29 Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model Gao, Han Huang, Ningjing Wang, Weiwei Zhang, Lingling Cai, Li Chen, Min Li, Wentao Med Sci Monit Animal Study BACKGROUND: Ischemic cerebrovascular disease leads to the activation and differentiation of neural stem cells (NSCs) into mature neurons and glia cells to repair nerve damage. Astragalus flavone (ASF) has shown its potential role in proliferation and differentiation into dopamine neurons of NSCs. MATERIAL/METHODS: Cerebral infarction models were constructed to determine the effects of ASF on NSCs in vivo and in vitro. RESULTS: ASF therapy had the ability to reduce the neurologic function scores and the cerebral infarction volume of the cerebral infarction model. Moreover, ASF was able to increase BrdU-positive cells and promote the expression of Nestin, β-Tubulin III, and O4, while decreasing the expression of GFAP. qRT-PCR and western blot assays showed ASF promoted the expression of Mash1, Math1, and Ngn2 mRNA and protein in cerebral infarction rats. Meanwhile, ASF (20 μg/ml) was able to increase EdU-positive cells and promote the expression of Nestin, β-Tubulin III, and O4 of NSCs at day14 in vitro. In normoxia, ASF obviously promoted the expression of Mash1, Ngn1, and Ngn2 mRNA and proteins, but in hypoxia, ASF promoted the expression of Notch1 and Math1 mRNA and proteins and inhibited the expression of Ngn1 and Ngn2 mRNA and proteins. CONCLUSIONS: ASF therapy can improve the neurologic functions and reduce the cerebral infarction volume in a cerebral infarction model. Moreover, ASF promoted the proliferation of NSCs and induced differentiation into neurons and oligodendrocytes, which might be involved in regulating factors in Notch signaling. International Scientific Literature, Inc. 2022-03-07 /pmc/articles/PMC8915658/ /pubmed/35250022 http://dx.doi.org/10.12659/MSM.933830 Text en © Med Sci Monit, 2022 https://creativecommons.org/licenses/by-nc-nd/4.0/This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) ) |
spellingShingle | Animal Study Gao, Han Huang, Ningjing Wang, Weiwei Zhang, Lingling Cai, Li Chen, Min Li, Wentao Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model |
title | Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model |
title_full | Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model |
title_fullStr | Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model |
title_full_unstemmed | Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model |
title_short | Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model |
title_sort | astragalus flavone induces proliferation and differentiation of neural stem cells in a cerebral infarction model |
topic | Animal Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8915658/ https://www.ncbi.nlm.nih.gov/pubmed/35250022 http://dx.doi.org/10.12659/MSM.933830 |
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