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Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression
β-amyloid formation in the brain is one of the characteristics of Alzheimer’s disease. Exposure to this peptide may result in reentry into the cell cycle leading to cell death. The phytoestrogen equol has similar biological effects as estrogen without the side effects. This study investigated the po...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6835339/ https://www.ncbi.nlm.nih.gov/pubmed/31623342 http://dx.doi.org/10.3390/nu11102356 |
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author | Tsai, Meng-Chao Lin, Shyh-Hsiang Hidayah, Kiswatul Lin, Ching-I |
author_facet | Tsai, Meng-Chao Lin, Shyh-Hsiang Hidayah, Kiswatul Lin, Ching-I |
author_sort | Tsai, Meng-Chao |
collection | PubMed |
description | β-amyloid formation in the brain is one of the characteristics of Alzheimer’s disease. Exposure to this peptide may result in reentry into the cell cycle leading to cell death. The phytoestrogen equol has similar biological effects as estrogen without the side effects. This study investigated the possible mechanism of the neuron cell-protecting effect of equol during treatment with Aβ. SH-SY5Y neuroblastoma cells were treated with either 1 μM S-equol or 10 nM 17β-estradiol for 24 h prior to 1 μM Aβ (25–35) exposure. After 24 h exposure to Aβ (25–35), a significant reduction in cell survival and a reentry into the cell cycle process accompanied by increased levels of cyclin D1 were observed. The expressions of estrogen receptor alpha (ERα) and its coactivator, steroid receptor coactivator-1 (SRC-1), were also significantly downregulated by Aβ (25–35) in parallel with activated extracellular signal-regulated kinase (ERK)1/2. However, pretreatment of cells with S-equol or 17β-estradiol reversed these effects. Treatment with the ER antagonist, ICI-182,780 (1 μM), completely blocked the effects of S-equol and 17β-estradiol on cell viability, ERα, and ERK1/2 after Aβ (25–35) exposure. These data suggest that S-equol possesses a neuroprotective potential as it effectively antagonizes Aβ (25–35)-induced cell cytotoxicity and prevents cell cycle reentry in SH-SY5Y cells. The mechanism underlying S-equol neuroprotection might involve ERα-mediated pathways. |
format | Online Article Text |
id | pubmed-6835339 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-68353392019-11-25 Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression Tsai, Meng-Chao Lin, Shyh-Hsiang Hidayah, Kiswatul Lin, Ching-I Nutrients Article β-amyloid formation in the brain is one of the characteristics of Alzheimer’s disease. Exposure to this peptide may result in reentry into the cell cycle leading to cell death. The phytoestrogen equol has similar biological effects as estrogen without the side effects. This study investigated the possible mechanism of the neuron cell-protecting effect of equol during treatment with Aβ. SH-SY5Y neuroblastoma cells were treated with either 1 μM S-equol or 10 nM 17β-estradiol for 24 h prior to 1 μM Aβ (25–35) exposure. After 24 h exposure to Aβ (25–35), a significant reduction in cell survival and a reentry into the cell cycle process accompanied by increased levels of cyclin D1 were observed. The expressions of estrogen receptor alpha (ERα) and its coactivator, steroid receptor coactivator-1 (SRC-1), were also significantly downregulated by Aβ (25–35) in parallel with activated extracellular signal-regulated kinase (ERK)1/2. However, pretreatment of cells with S-equol or 17β-estradiol reversed these effects. Treatment with the ER antagonist, ICI-182,780 (1 μM), completely blocked the effects of S-equol and 17β-estradiol on cell viability, ERα, and ERK1/2 after Aβ (25–35) exposure. These data suggest that S-equol possesses a neuroprotective potential as it effectively antagonizes Aβ (25–35)-induced cell cytotoxicity and prevents cell cycle reentry in SH-SY5Y cells. The mechanism underlying S-equol neuroprotection might involve ERα-mediated pathways. MDPI 2019-10-03 /pmc/articles/PMC6835339/ /pubmed/31623342 http://dx.doi.org/10.3390/nu11102356 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Tsai, Meng-Chao Lin, Shyh-Hsiang Hidayah, Kiswatul Lin, Ching-I Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression |
title | Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression |
title_full | Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression |
title_fullStr | Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression |
title_full_unstemmed | Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression |
title_short | Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression |
title_sort | equol pretreatment protection of sh-sy5y cells against aβ (25–35)-induced cytotoxicity and cell-cycle reentry via sustaining estrogen receptor alpha expression |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6835339/ https://www.ncbi.nlm.nih.gov/pubmed/31623342 http://dx.doi.org/10.3390/nu11102356 |
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