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Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals
Recent evidence shows that the gut microbiota has an important role in gut-brain crosstalk and is linked to neuronal disorders. The aim of this study was to investigate the effects of intestinal Ruminococcus albus with probiotic potential on neuroprotection in oxidatively stressed SH-SY5Y neuroblast...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5674049/ https://www.ncbi.nlm.nih.gov/pubmed/29109537 http://dx.doi.org/10.1038/s41598-017-15163-5 |
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author | Park, Jieun Lee, Jiyun Yeom, Zia Heo, Donghyuk Lim, Young-Hee |
author_facet | Park, Jieun Lee, Jiyun Yeom, Zia Heo, Donghyuk Lim, Young-Hee |
author_sort | Park, Jieun |
collection | PubMed |
description | Recent evidence shows that the gut microbiota has an important role in gut-brain crosstalk and is linked to neuronal disorders. The aim of this study was to investigate the effects of intestinal Ruminococcus albus with probiotic potential on neuroprotection in oxidatively stressed SH-SY5Y neuroblastoma cells and animals. To investigate these effects, conditioned medium was prepared using Caco-2 cells cultured with heat-killed R. albus (CRA-CM). Caco-2 cells cultured with heat-killed R. albus showed increased BDNF expression and BDNF protein levels increased in CRA-CM. CRA-CM up-regulated the protein expression levels of SRF, C-fos and CDK2. In addition, CRA-CM protected SH-SY5Y cells from H(2)O(2)-induced cell death. CRA-CM significantly decreased the Bax/Bcl-2 ratio in oxidatively stressed SH-SY5Y cells. Animal experiments showed that oral administration of heat-killed R. albus for 15 days attenuated the oxidative stress induced by sodium arsenate. Treatment with heat-killed R. albus reduced the level of ROS, and the levels of SOD and GSH increased in oxidatively stressed brains. In conclusion, the secretome prepared from Caco-2 cells cultured with heat-killed R. albus might promote neuronal proliferation through the activation of cell proliferation-related proteins, and heat-killed R. albus protects neurons from oxidative damage by reducing ROS levels and increasing SOD and GSH levels. |
format | Online Article Text |
id | pubmed-5674049 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-56740492017-11-15 Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals Park, Jieun Lee, Jiyun Yeom, Zia Heo, Donghyuk Lim, Young-Hee Sci Rep Article Recent evidence shows that the gut microbiota has an important role in gut-brain crosstalk and is linked to neuronal disorders. The aim of this study was to investigate the effects of intestinal Ruminococcus albus with probiotic potential on neuroprotection in oxidatively stressed SH-SY5Y neuroblastoma cells and animals. To investigate these effects, conditioned medium was prepared using Caco-2 cells cultured with heat-killed R. albus (CRA-CM). Caco-2 cells cultured with heat-killed R. albus showed increased BDNF expression and BDNF protein levels increased in CRA-CM. CRA-CM up-regulated the protein expression levels of SRF, C-fos and CDK2. In addition, CRA-CM protected SH-SY5Y cells from H(2)O(2)-induced cell death. CRA-CM significantly decreased the Bax/Bcl-2 ratio in oxidatively stressed SH-SY5Y cells. Animal experiments showed that oral administration of heat-killed R. albus for 15 days attenuated the oxidative stress induced by sodium arsenate. Treatment with heat-killed R. albus reduced the level of ROS, and the levels of SOD and GSH increased in oxidatively stressed brains. In conclusion, the secretome prepared from Caco-2 cells cultured with heat-killed R. albus might promote neuronal proliferation through the activation of cell proliferation-related proteins, and heat-killed R. albus protects neurons from oxidative damage by reducing ROS levels and increasing SOD and GSH levels. Nature Publishing Group UK 2017-11-06 /pmc/articles/PMC5674049/ /pubmed/29109537 http://dx.doi.org/10.1038/s41598-017-15163-5 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Park, Jieun Lee, Jiyun Yeom, Zia Heo, Donghyuk Lim, Young-Hee Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals |
title | Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals |
title_full | Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals |
title_fullStr | Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals |
title_full_unstemmed | Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals |
title_short | Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals |
title_sort | neuroprotective effect of ruminococcus albus on oxidatively stressed sh-sy5y cells and animals |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5674049/ https://www.ncbi.nlm.nih.gov/pubmed/29109537 http://dx.doi.org/10.1038/s41598-017-15163-5 |
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