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Antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via Wnt/β-Catenin pathway
BACKGROUND: Recently, the antioxidant properties of the natural compound, selenomethionine (Se-Met), have been recognized. However, its effect on the osteogenic mineralization of the Wnt/β-Catenin pathway under conditions of oxidative stress and inflammation remain unclear. METHODS: This study utili...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10594567/ https://www.ncbi.nlm.nih.gov/pubmed/37881410 http://dx.doi.org/10.1016/j.bbrep.2023.101559 |
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author | Zhao, Guodong Zhang, Yiting Tian, Yinping Huang, Jing Gao, Peiyi Zhao, Qin Yang, Zaibo |
author_facet | Zhao, Guodong Zhang, Yiting Tian, Yinping Huang, Jing Gao, Peiyi Zhao, Qin Yang, Zaibo |
author_sort | Zhao, Guodong |
collection | PubMed |
description | BACKGROUND: Recently, the antioxidant properties of the natural compound, selenomethionine (Se-Met), have been recognized. However, its effect on the osteogenic mineralization of the Wnt/β-Catenin pathway under conditions of oxidative stress and inflammation remain unclear. METHODS: This study utilized tert-butyl hydroperoxide (TBHP) to simulate oxidative stress and inflammation. Se-Met was then subsequently used to inhibit these effects in vitro. RESULTS: TBHP induces oxidative stress and inflammatory responses by increasing the expression of reactive oxygen species and NLRP3, whereas decreasing the expression of GPX4, thereby inhibiting the viability of MC3T3-E1 cells. TBHP further promotes lipid peroxidation and damages the ultrastructure of mitochondria. Furthermore, TBHP inhibits the expression levels of β-Catenin, thereby reducing the activity of the Wnt pathway, which in turn suppresses the osteogenic differentiation and mineralization capacity. Importantly, Se-Met significantly alters the aforementioned responses to enhance expression levels of Wnt pathway-related proteins and improving the osteogenic differentiation and mineralization capacity of the cells. CONCLUSION: Se-Met enhances antioxidant and anti-inflammatory responses in MC3T3-E1 cells via the Wnt/β-Catenin signaling pathway to promote osteogenesis. Thus, Se-Met plays a crucial role in the field of bone homeostasis, and presents an opportunity for the future development of novel drugs for treating osteoporosis and maintaining bone stability. However, further detailed preclinical animal studies are required to generate solid and reliable data to aid this development. |
format | Online Article Text |
id | pubmed-10594567 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-105945672023-10-25 Antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via Wnt/β-Catenin pathway Zhao, Guodong Zhang, Yiting Tian, Yinping Huang, Jing Gao, Peiyi Zhao, Qin Yang, Zaibo Biochem Biophys Rep Research Article BACKGROUND: Recently, the antioxidant properties of the natural compound, selenomethionine (Se-Met), have been recognized. However, its effect on the osteogenic mineralization of the Wnt/β-Catenin pathway under conditions of oxidative stress and inflammation remain unclear. METHODS: This study utilized tert-butyl hydroperoxide (TBHP) to simulate oxidative stress and inflammation. Se-Met was then subsequently used to inhibit these effects in vitro. RESULTS: TBHP induces oxidative stress and inflammatory responses by increasing the expression of reactive oxygen species and NLRP3, whereas decreasing the expression of GPX4, thereby inhibiting the viability of MC3T3-E1 cells. TBHP further promotes lipid peroxidation and damages the ultrastructure of mitochondria. Furthermore, TBHP inhibits the expression levels of β-Catenin, thereby reducing the activity of the Wnt pathway, which in turn suppresses the osteogenic differentiation and mineralization capacity. Importantly, Se-Met significantly alters the aforementioned responses to enhance expression levels of Wnt pathway-related proteins and improving the osteogenic differentiation and mineralization capacity of the cells. CONCLUSION: Se-Met enhances antioxidant and anti-inflammatory responses in MC3T3-E1 cells via the Wnt/β-Catenin signaling pathway to promote osteogenesis. Thus, Se-Met plays a crucial role in the field of bone homeostasis, and presents an opportunity for the future development of novel drugs for treating osteoporosis and maintaining bone stability. However, further detailed preclinical animal studies are required to generate solid and reliable data to aid this development. Elsevier 2023-10-18 /pmc/articles/PMC10594567/ /pubmed/37881410 http://dx.doi.org/10.1016/j.bbrep.2023.101559 Text en © 2023 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Research Article Zhao, Guodong Zhang, Yiting Tian, Yinping Huang, Jing Gao, Peiyi Zhao, Qin Yang, Zaibo Antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via Wnt/β-Catenin pathway |
title | Antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via Wnt/β-Catenin pathway |
title_full | Antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via Wnt/β-Catenin pathway |
title_fullStr | Antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via Wnt/β-Catenin pathway |
title_full_unstemmed | Antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via Wnt/β-Catenin pathway |
title_short | Antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via Wnt/β-Catenin pathway |
title_sort | antioxidant and anti-inflammatory effects of selenomethionine promote osteogenesis via wnt/β-catenin pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10594567/ https://www.ncbi.nlm.nih.gov/pubmed/37881410 http://dx.doi.org/10.1016/j.bbrep.2023.101559 |
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