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Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans
Amyloid-β, a hallmark of Alzheimer’s disease, forms toxic intracellular oligomers and extracellular senile plaques resulting in neuronal toxicity. Ethanol is widely consumed worldwide. Moderate ethanol consumption has numerous benefits in humans. We found that ethanol could significantly extend the...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632871/ https://www.ncbi.nlm.nih.gov/pubmed/34867289 http://dx.doi.org/10.3389/fnagi.2021.762659 |
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author | Bai, Shuju Wang, Wenbo Zhang, Zhiwei Li, Mengyao Chen, Zehan Wang, Jiuqiao Zhao, Yanlin An, Lu Wang, Yuxiang Xing, Shu Fu, Xueqi Ma, Junfeng |
author_facet | Bai, Shuju Wang, Wenbo Zhang, Zhiwei Li, Mengyao Chen, Zehan Wang, Jiuqiao Zhao, Yanlin An, Lu Wang, Yuxiang Xing, Shu Fu, Xueqi Ma, Junfeng |
author_sort | Bai, Shuju |
collection | PubMed |
description | Amyloid-β, a hallmark of Alzheimer’s disease, forms toxic intracellular oligomers and extracellular senile plaques resulting in neuronal toxicity. Ethanol is widely consumed worldwide. Moderate ethanol consumption has numerous benefits in humans. We found that ethanol could significantly extend the lifespan of Caenorhabiditis elegans in a previous study. Based on that study, we tested the effect of ethanol on Alzheimer’s disease transgenic Caenorhabiditis elegans strain CL4176, which expresses amyloid-β1-42 peptide in body wall muscle cells. Ethanol delayed paralysis and reduced amyloid-β oligomers in Caenorhabiditis elegans worms of the CL4176 strain. Moreover, ethanol could induce the nuclear translocation of DAF-16 in the nematodes. However, in worms that were fed daf-16 RNAi bacteria, ethanol no longer delayed the paralysis. The qPCR assays showed that ethanol increases the expression of daf-16, hsf-1 and their common target genes- small heat shock protein genes. In addition, we also found that ethanol could increase lysosome mass in the CL4176 worms. In summary, our study indicated that ethanol attenuated amyloid-β toxicity in the Alzheimer’s disease model of Caenorhabiditis elegans via increasing the level of lysosomes to promote amyloid-β degradation and upregulating the levels of small heat shock protein genes to reduce amyloid-β aggregation. |
format | Online Article Text |
id | pubmed-8632871 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86328712021-12-02 Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans Bai, Shuju Wang, Wenbo Zhang, Zhiwei Li, Mengyao Chen, Zehan Wang, Jiuqiao Zhao, Yanlin An, Lu Wang, Yuxiang Xing, Shu Fu, Xueqi Ma, Junfeng Front Aging Neurosci Neuroscience Amyloid-β, a hallmark of Alzheimer’s disease, forms toxic intracellular oligomers and extracellular senile plaques resulting in neuronal toxicity. Ethanol is widely consumed worldwide. Moderate ethanol consumption has numerous benefits in humans. We found that ethanol could significantly extend the lifespan of Caenorhabiditis elegans in a previous study. Based on that study, we tested the effect of ethanol on Alzheimer’s disease transgenic Caenorhabiditis elegans strain CL4176, which expresses amyloid-β1-42 peptide in body wall muscle cells. Ethanol delayed paralysis and reduced amyloid-β oligomers in Caenorhabiditis elegans worms of the CL4176 strain. Moreover, ethanol could induce the nuclear translocation of DAF-16 in the nematodes. However, in worms that were fed daf-16 RNAi bacteria, ethanol no longer delayed the paralysis. The qPCR assays showed that ethanol increases the expression of daf-16, hsf-1 and their common target genes- small heat shock protein genes. In addition, we also found that ethanol could increase lysosome mass in the CL4176 worms. In summary, our study indicated that ethanol attenuated amyloid-β toxicity in the Alzheimer’s disease model of Caenorhabiditis elegans via increasing the level of lysosomes to promote amyloid-β degradation and upregulating the levels of small heat shock protein genes to reduce amyloid-β aggregation. Frontiers Media S.A. 2021-11-12 /pmc/articles/PMC8632871/ /pubmed/34867289 http://dx.doi.org/10.3389/fnagi.2021.762659 Text en Copyright © 2021 Bai, Wang, Zhang, Li, Chen, Wang, Zhao, An, Wang, Xing, Fu and Ma. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Bai, Shuju Wang, Wenbo Zhang, Zhiwei Li, Mengyao Chen, Zehan Wang, Jiuqiao Zhao, Yanlin An, Lu Wang, Yuxiang Xing, Shu Fu, Xueqi Ma, Junfeng Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans |
title | Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans |
title_full | Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans |
title_fullStr | Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans |
title_full_unstemmed | Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans |
title_short | Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans |
title_sort | ethanol alleviates amyloid-β-induced toxicity in an alzheimer’s disease model of caenorhabiditis elegans |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632871/ https://www.ncbi.nlm.nih.gov/pubmed/34867289 http://dx.doi.org/10.3389/fnagi.2021.762659 |
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