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Tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating PU.1 expression
Inhibiting β-amyloid (Aβ)-induced microglial activation is proposed as an effective strategy for the treatment of Alzheimer’s disease. Tetrahydroxystilbene glycoside (TSG) is the main active ingredient of Polygonum multiflorum and has a wide range of biological properties, including antiinflammation...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Lippincott Williams & Wilkins
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5999375/ https://www.ncbi.nlm.nih.gov/pubmed/29668503 http://dx.doi.org/10.1097/WNR.0000000000001032 |
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author | Jiao, Chenli Gao, Feng Ou, Li Yu, Jinhua Li, Min Wei, Peifeng Miu, Feng |
author_facet | Jiao, Chenli Gao, Feng Ou, Li Yu, Jinhua Li, Min Wei, Peifeng Miu, Feng |
author_sort | Jiao, Chenli |
collection | PubMed |
description | Inhibiting β-amyloid (Aβ)-induced microglial activation is proposed as an effective strategy for the treatment of Alzheimer’s disease. Tetrahydroxystilbene glycoside (TSG) is the main active ingredient of Polygonum multiflorum and has a wide range of biological properties, including antiinflammation. Here, we focused on the function and regulatory mechanism of TSG in Aβ-induced N9 and BV2 cells. The results showed that Aβ treatment induced the activation of microglia cells and the production of inflammatory molecules, including inducible nitric oxide synthase, nitric oxide, cyclooxygenase 2, and prostaglandin E2, which were significantly inhibited by TSG pretreatment. Furthermore, we found Aβ exposure increased the levels of microglial M1 markers, interleukin (IL)-1β, IL-6, and tumor necrosis factor α, and the pretreatment of TSG suppressed the increase of M1 markers and enhanced the levels of M2 markers, including IL-10, brain-derived neurotrophic factor, glial cell-derived neurotrophic factor, and arginase-1. PU.1 overexpression was found to eradicate the anti-inflammatory effects of TSG in Aβ-induced microglial cells. Taken together, these findings indicate that TSG attenuates Aβ-induced microglial activation and polarizes microglia towards M2 phenotype, which may be closely associated with the regulation of PU.1. |
format | Online Article Text |
id | pubmed-5999375 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Lippincott Williams & Wilkins |
record_format | MEDLINE/PubMed |
spelling | pubmed-59993752018-06-19 Tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating PU.1 expression Jiao, Chenli Gao, Feng Ou, Li Yu, Jinhua Li, Min Wei, Peifeng Miu, Feng Neuroreport Cellular, Molecular and Developmental Neuroscience Inhibiting β-amyloid (Aβ)-induced microglial activation is proposed as an effective strategy for the treatment of Alzheimer’s disease. Tetrahydroxystilbene glycoside (TSG) is the main active ingredient of Polygonum multiflorum and has a wide range of biological properties, including antiinflammation. Here, we focused on the function and regulatory mechanism of TSG in Aβ-induced N9 and BV2 cells. The results showed that Aβ treatment induced the activation of microglia cells and the production of inflammatory molecules, including inducible nitric oxide synthase, nitric oxide, cyclooxygenase 2, and prostaglandin E2, which were significantly inhibited by TSG pretreatment. Furthermore, we found Aβ exposure increased the levels of microglial M1 markers, interleukin (IL)-1β, IL-6, and tumor necrosis factor α, and the pretreatment of TSG suppressed the increase of M1 markers and enhanced the levels of M2 markers, including IL-10, brain-derived neurotrophic factor, glial cell-derived neurotrophic factor, and arginase-1. PU.1 overexpression was found to eradicate the anti-inflammatory effects of TSG in Aβ-induced microglial cells. Taken together, these findings indicate that TSG attenuates Aβ-induced microglial activation and polarizes microglia towards M2 phenotype, which may be closely associated with the regulation of PU.1. Lippincott Williams & Wilkins 2018-07-04 2018-06-06 /pmc/articles/PMC5999375/ /pubmed/29668503 http://dx.doi.org/10.1097/WNR.0000000000001032 Text en Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved. |
spellingShingle | Cellular, Molecular and Developmental Neuroscience Jiao, Chenli Gao, Feng Ou, Li Yu, Jinhua Li, Min Wei, Peifeng Miu, Feng Tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating PU.1 expression |
title | Tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating PU.1 expression |
title_full | Tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating PU.1 expression |
title_fullStr | Tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating PU.1 expression |
title_full_unstemmed | Tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating PU.1 expression |
title_short | Tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating PU.1 expression |
title_sort | tetrahydroxystilbene glycoside antagonizes β-amyloid-induced inflammatory injury in microglia cells by regulating pu.1 expression |
topic | Cellular, Molecular and Developmental Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5999375/ https://www.ncbi.nlm.nih.gov/pubmed/29668503 http://dx.doi.org/10.1097/WNR.0000000000001032 |
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