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Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity
Excess extracellular glutamate leads to excitotoxicity, which induces neuronal death through the overactivation of N-methyl-D-aspartate receptors (NMDARs). Excitotoxicity is thought to be closely related to various acute and chronic neurological disorders, such as stroke and Alzheimer’s disease. Pol...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8451577/ https://www.ncbi.nlm.nih.gov/pubmed/34100454 http://dx.doi.org/10.4103/1673-5374.314321 |
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author | Sun, Chong Cao, Xin-Cheng Liu, Zhi-Yang Ma, Chao-Lin Li, Bao-Ming |
author_facet | Sun, Chong Cao, Xin-Cheng Liu, Zhi-Yang Ma, Chao-Lin Li, Bao-Ming |
author_sort | Sun, Chong |
collection | PubMed |
description | Excess extracellular glutamate leads to excitotoxicity, which induces neuronal death through the overactivation of N-methyl-D-aspartate receptors (NMDARs). Excitotoxicity is thought to be closely related to various acute and chronic neurological disorders, such as stroke and Alzheimer’s disease. Polygalasaponin F (PGSF) is a triterpenoid saponin monomer that can be isolated from Polygala japonica, and has been reported to protect cells against apoptosis. To investigate the mechanisms underlying the neuroprotective effects of PGSF against glutamate-induced cytotoxicity, PGSF-pretreated hippocampal neurons were exposed to glutamate for 24 hours. The results demonstrated that PGSF inhibited glutamate-induced hippocampal neuron death in a concentration-dependent manner and reduced glutamate-induced Ca(2+) overload in the cultured neurons. In addition, PGSF partially blocked the excess activity of NMDARs, inhibited both the downregulation of NMDAR subunit NR2A expression and the upregulation of NMDAR subunit NR2B expression, and upregulated the expression of phosphorylated cyclic adenosine monophosphate-responsive element-binding protein and brain-derived neurotrophic factor. These findings suggest that PGSF protects cultured hippocampal neurons against glutamate-induced cytotoxicity by regulating NMDARs. The study was approved by the Institutional Animal Care Committee of Nanchang University (approval No. 2017-0006) on December 29, 2017. |
format | Online Article Text |
id | pubmed-8451577 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-84515772021-10-18 Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity Sun, Chong Cao, Xin-Cheng Liu, Zhi-Yang Ma, Chao-Lin Li, Bao-Ming Neural Regen Res Research Article Excess extracellular glutamate leads to excitotoxicity, which induces neuronal death through the overactivation of N-methyl-D-aspartate receptors (NMDARs). Excitotoxicity is thought to be closely related to various acute and chronic neurological disorders, such as stroke and Alzheimer’s disease. Polygalasaponin F (PGSF) is a triterpenoid saponin monomer that can be isolated from Polygala japonica, and has been reported to protect cells against apoptosis. To investigate the mechanisms underlying the neuroprotective effects of PGSF against glutamate-induced cytotoxicity, PGSF-pretreated hippocampal neurons were exposed to glutamate for 24 hours. The results demonstrated that PGSF inhibited glutamate-induced hippocampal neuron death in a concentration-dependent manner and reduced glutamate-induced Ca(2+) overload in the cultured neurons. In addition, PGSF partially blocked the excess activity of NMDARs, inhibited both the downregulation of NMDAR subunit NR2A expression and the upregulation of NMDAR subunit NR2B expression, and upregulated the expression of phosphorylated cyclic adenosine monophosphate-responsive element-binding protein and brain-derived neurotrophic factor. These findings suggest that PGSF protects cultured hippocampal neurons against glutamate-induced cytotoxicity by regulating NMDARs. The study was approved by the Institutional Animal Care Committee of Nanchang University (approval No. 2017-0006) on December 29, 2017. Wolters Kluwer - Medknow 2021-06-07 /pmc/articles/PMC8451577/ /pubmed/34100454 http://dx.doi.org/10.4103/1673-5374.314321 Text en Copyright: © Neural Regeneration Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Research Article Sun, Chong Cao, Xin-Cheng Liu, Zhi-Yang Ma, Chao-Lin Li, Bao-Ming Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity |
title | Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity |
title_full | Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity |
title_fullStr | Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity |
title_full_unstemmed | Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity |
title_short | Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity |
title_sort | polygalasaponin f protects hippocampal neurons against glutamate-induced cytotoxicity |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8451577/ https://www.ncbi.nlm.nih.gov/pubmed/34100454 http://dx.doi.org/10.4103/1673-5374.314321 |
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