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Neuroprotective properties of queen bee acid by autophagy induction
Autophagy is a conserved intracellular catabolic pathway that removes cytoplasmic components to contribute to neuronal homeostasis. Accumulating evidence has increasingly shown that the induction of autophagy improves neuronal health and extends longevity in several animal models. Therefore, there i...
Autores principales: | , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Netherlands
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10406658/ https://www.ncbi.nlm.nih.gov/pubmed/34448959 http://dx.doi.org/10.1007/s10565-021-09625-w |
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author | Martínez-Chacón, Guadalupe Paredes-Barquero, Marta Yakhine-Diop, Sokhna M.S Uribe-Carretero, Elisabet Bargiela, Ariadna Sabater-Arcis, María Morales-García, José Alarcón-Gil, Jesús Alegre-Cortés, Eva Canales-Cortés, Saray Rodríguez-Arribas, Mario Camello, Pedro Javier Pedro, José Manuel Bravo-San Perez-Castillo, Ana Artero, Rubén Gonzalez-Polo, Rosa A. Fuentes, José M. Niso-Santano, Mireia |
author_facet | Martínez-Chacón, Guadalupe Paredes-Barquero, Marta Yakhine-Diop, Sokhna M.S Uribe-Carretero, Elisabet Bargiela, Ariadna Sabater-Arcis, María Morales-García, José Alarcón-Gil, Jesús Alegre-Cortés, Eva Canales-Cortés, Saray Rodríguez-Arribas, Mario Camello, Pedro Javier Pedro, José Manuel Bravo-San Perez-Castillo, Ana Artero, Rubén Gonzalez-Polo, Rosa A. Fuentes, José M. Niso-Santano, Mireia |
author_sort | Martínez-Chacón, Guadalupe |
collection | PubMed |
description | Autophagy is a conserved intracellular catabolic pathway that removes cytoplasmic components to contribute to neuronal homeostasis. Accumulating evidence has increasingly shown that the induction of autophagy improves neuronal health and extends longevity in several animal models. Therefore, there is a great interest in the identification of effective autophagy enhancers with potential nutraceutical or pharmaceutical properties to ameliorate age-related diseases, such as neurodegenerative disorders, and/or promote longevity. Queen bee acid (QBA, 10-hydroxy-2-decenoic acid) is the major fatty acid component of, and is found exclusively in, royal jelly, which has beneficial properties for human health. It is reported that QBA has antitumor, anti-inflammatory, and antibacterial activities and promotes neurogenesis and neuronal health; however, the mechanism by which QBA exerts these effects has not been fully elucidated. The present study investigated the role of the autophagic process in the protective effect of QBA. We found that QBA is a novel autophagy inducer that triggers autophagy in various neuronal cell lines and mouse and fly models. The beclin-1 (BECN1) and mTOR pathways participate in the regulation of QBA-induced autophagy. Moreover, our results showed that QBA stimulates sirtuin 1 (SIRT1), which promotes autophagy by the deacetylation of critical ATG proteins. Finally, QBA-mediated autophagy promotes neuroprotection in Parkinson’s disease in vitro and in a mouse model and extends the lifespan of Drosophila melanogaster. This study provides detailed evidences showing that autophagy induction plays a critical role in the beneficial health effects of QBA. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10565-021-09625-w. |
format | Online Article Text |
id | pubmed-10406658 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
spelling | pubmed-104066582023-08-09 Neuroprotective properties of queen bee acid by autophagy induction Martínez-Chacón, Guadalupe Paredes-Barquero, Marta Yakhine-Diop, Sokhna M.S Uribe-Carretero, Elisabet Bargiela, Ariadna Sabater-Arcis, María Morales-García, José Alarcón-Gil, Jesús Alegre-Cortés, Eva Canales-Cortés, Saray Rodríguez-Arribas, Mario Camello, Pedro Javier Pedro, José Manuel Bravo-San Perez-Castillo, Ana Artero, Rubén Gonzalez-Polo, Rosa A. Fuentes, José M. Niso-Santano, Mireia Cell Biol Toxicol Original Article Autophagy is a conserved intracellular catabolic pathway that removes cytoplasmic components to contribute to neuronal homeostasis. Accumulating evidence has increasingly shown that the induction of autophagy improves neuronal health and extends longevity in several animal models. Therefore, there is a great interest in the identification of effective autophagy enhancers with potential nutraceutical or pharmaceutical properties to ameliorate age-related diseases, such as neurodegenerative disorders, and/or promote longevity. Queen bee acid (QBA, 10-hydroxy-2-decenoic acid) is the major fatty acid component of, and is found exclusively in, royal jelly, which has beneficial properties for human health. It is reported that QBA has antitumor, anti-inflammatory, and antibacterial activities and promotes neurogenesis and neuronal health; however, the mechanism by which QBA exerts these effects has not been fully elucidated. The present study investigated the role of the autophagic process in the protective effect of QBA. We found that QBA is a novel autophagy inducer that triggers autophagy in various neuronal cell lines and mouse and fly models. The beclin-1 (BECN1) and mTOR pathways participate in the regulation of QBA-induced autophagy. Moreover, our results showed that QBA stimulates sirtuin 1 (SIRT1), which promotes autophagy by the deacetylation of critical ATG proteins. Finally, QBA-mediated autophagy promotes neuroprotection in Parkinson’s disease in vitro and in a mouse model and extends the lifespan of Drosophila melanogaster. This study provides detailed evidences showing that autophagy induction plays a critical role in the beneficial health effects of QBA. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10565-021-09625-w. Springer Netherlands 2021-08-27 2023 /pmc/articles/PMC10406658/ /pubmed/34448959 http://dx.doi.org/10.1007/s10565-021-09625-w Text en © The Author(s) 2021 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 | Original Article Martínez-Chacón, Guadalupe Paredes-Barquero, Marta Yakhine-Diop, Sokhna M.S Uribe-Carretero, Elisabet Bargiela, Ariadna Sabater-Arcis, María Morales-García, José Alarcón-Gil, Jesús Alegre-Cortés, Eva Canales-Cortés, Saray Rodríguez-Arribas, Mario Camello, Pedro Javier Pedro, José Manuel Bravo-San Perez-Castillo, Ana Artero, Rubén Gonzalez-Polo, Rosa A. Fuentes, José M. Niso-Santano, Mireia Neuroprotective properties of queen bee acid by autophagy induction |
title | Neuroprotective properties of queen bee acid by autophagy induction |
title_full | Neuroprotective properties of queen bee acid by autophagy induction |
title_fullStr | Neuroprotective properties of queen bee acid by autophagy induction |
title_full_unstemmed | Neuroprotective properties of queen bee acid by autophagy induction |
title_short | Neuroprotective properties of queen bee acid by autophagy induction |
title_sort | neuroprotective properties of queen bee acid by autophagy induction |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10406658/ https://www.ncbi.nlm.nih.gov/pubmed/34448959 http://dx.doi.org/10.1007/s10565-021-09625-w |
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