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Exosomes secreted by mesenchymal stem cells delay brain aging by upregulating SIRT1 expression
The increase in the aging population has seriously affected our society. Neurodegenerative diseases caused by aging of the brain significantly impact the normal life of the elderly, and delaying brain aging is currently the focus of research. SIRT1 is a viable therapeutic target, and there is mounti...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10425430/ https://www.ncbi.nlm.nih.gov/pubmed/37580391 http://dx.doi.org/10.1038/s41598-023-40543-5 |
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author | Zhang, Xiaowen Liu, Te Hou, Xuejia Zhou, Zhongsheng Zhang, Fuqiang Ma, He Wu, Xiaodong Jiang, Jinlan |
author_facet | Zhang, Xiaowen Liu, Te Hou, Xuejia Zhou, Zhongsheng Zhang, Fuqiang Ma, He Wu, Xiaodong Jiang, Jinlan |
author_sort | Zhang, Xiaowen |
collection | PubMed |
description | The increase in the aging population has seriously affected our society. Neurodegenerative diseases caused by aging of the brain significantly impact the normal life of the elderly, and delaying brain aging is currently the focus of research. SIRT1 is a viable therapeutic target, and there is mounting evidence that it plays a significant role in the aging process. Mesenchymal stem cell-derived exosomes (MSC-Exos) have gained widespread interest as nanotherapeutic agents because of their ability to be injected at high doses to reduce the immune response. The present study focused on the ameliorative effect of MSC-Exos on aging mice and the potential mechanisms of this effect on cognitive impairment and brain aging. In this study, we first tested the neuroprotective effects of MSC-Exos in vitro on H(2)O(2)-induced oxidative damage in BV2 cells. An in vivo SAMP8 rapid senescence mouse model showed that MSC-Exos significantly increased SIRT1 gene expression in senescent mice. In addition, MSC-Exos also had an anti-apoptotic effect and reduced oxidative stress in the brains of SAMP8 senescent mice. In conclusion, MSC-Exos may exert neuroprotective effects and help prevent brain senescence in SAMP8 mice by activating the SIRT1 signaling pathway. |
format | Online Article Text |
id | pubmed-10425430 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-104254302023-08-16 Exosomes secreted by mesenchymal stem cells delay brain aging by upregulating SIRT1 expression Zhang, Xiaowen Liu, Te Hou, Xuejia Zhou, Zhongsheng Zhang, Fuqiang Ma, He Wu, Xiaodong Jiang, Jinlan Sci Rep Article The increase in the aging population has seriously affected our society. Neurodegenerative diseases caused by aging of the brain significantly impact the normal life of the elderly, and delaying brain aging is currently the focus of research. SIRT1 is a viable therapeutic target, and there is mounting evidence that it plays a significant role in the aging process. Mesenchymal stem cell-derived exosomes (MSC-Exos) have gained widespread interest as nanotherapeutic agents because of their ability to be injected at high doses to reduce the immune response. The present study focused on the ameliorative effect of MSC-Exos on aging mice and the potential mechanisms of this effect on cognitive impairment and brain aging. In this study, we first tested the neuroprotective effects of MSC-Exos in vitro on H(2)O(2)-induced oxidative damage in BV2 cells. An in vivo SAMP8 rapid senescence mouse model showed that MSC-Exos significantly increased SIRT1 gene expression in senescent mice. In addition, MSC-Exos also had an anti-apoptotic effect and reduced oxidative stress in the brains of SAMP8 senescent mice. In conclusion, MSC-Exos may exert neuroprotective effects and help prevent brain senescence in SAMP8 mice by activating the SIRT1 signaling pathway. Nature Publishing Group UK 2023-08-14 /pmc/articles/PMC10425430/ /pubmed/37580391 http://dx.doi.org/10.1038/s41598-023-40543-5 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Zhang, Xiaowen Liu, Te Hou, Xuejia Zhou, Zhongsheng Zhang, Fuqiang Ma, He Wu, Xiaodong Jiang, Jinlan Exosomes secreted by mesenchymal stem cells delay brain aging by upregulating SIRT1 expression |
title | Exosomes secreted by mesenchymal stem cells delay brain aging by upregulating SIRT1 expression |
title_full | Exosomes secreted by mesenchymal stem cells delay brain aging by upregulating SIRT1 expression |
title_fullStr | Exosomes secreted by mesenchymal stem cells delay brain aging by upregulating SIRT1 expression |
title_full_unstemmed | Exosomes secreted by mesenchymal stem cells delay brain aging by upregulating SIRT1 expression |
title_short | Exosomes secreted by mesenchymal stem cells delay brain aging by upregulating SIRT1 expression |
title_sort | exosomes secreted by mesenchymal stem cells delay brain aging by upregulating sirt1 expression |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10425430/ https://www.ncbi.nlm.nih.gov/pubmed/37580391 http://dx.doi.org/10.1038/s41598-023-40543-5 |
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