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Cyanidin-3-glucoside Regulates Osteoblast Differentiation via the ERK1/2 Signaling Pathway
[Image: see text] Osteoporosis, characterized by a gradual decrease in the number of osteoblasts and a gradual increase in bone resorption of osteoclasts in bone tissue, is a global chronic disease, which severely impairs the quality of life of the elderly. Therefore, it is extremely urgent to study...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Chemical Society
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905819/ https://www.ncbi.nlm.nih.gov/pubmed/33644583 http://dx.doi.org/10.1021/acsomega.0c05603 |
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author | Hu, Bosen Chen, Lin Chen, Yong Zhang, Zhuo Wang, Xiaohong Zhou, Bo |
author_facet | Hu, Bosen Chen, Lin Chen, Yong Zhang, Zhuo Wang, Xiaohong Zhou, Bo |
author_sort | Hu, Bosen |
collection | PubMed |
description | [Image: see text] Osteoporosis, characterized by a gradual decrease in the number of osteoblasts and a gradual increase in bone resorption of osteoclasts in bone tissue, is a global chronic disease, which severely impairs the quality of life of the elderly. Therefore, it is extremely urgent to study the prevention and treatment of osteoporosis. It has been reported that anthocyanins can regulate bone metabolism and prevent osteoporosis. Cyanidin-3-O-glucoside (C3G), the most common type of anthocyanin in nature, widely exists in a variety of vegetables and fruits. Although it has been shown that C3G has multiple effects on osteoclasts, its impact(s) and underlying mechanism(s) on osteoblasts are still not clear. Here, we evaluated the effect of C3G on cell proliferation and differentiation of osteoblasts (extracted from the hip joint of patients with osteoporosis) and MC3T3-E1 (a kind of osteoblast cell line from mice). We also test the ability of osteoblasts to mineralize after C3G treatment. To find the underlying mechanism of the above effects, we further evaluated the role of the ERK signaling pathway in C3G regulation of osteoblasts. The results showed that C3G treatment enhanced osteoblast proliferation rate, osteoblast mineralization points, the mRNA levels and protein expression levels of OC (osteocalcin), and the level of ERK phosphorylation, which could be blocked by pretreatment with ERK signaling pathway inhibitor. The above results not only indicate that the ERK pathway was involved in C3G regulation of osteoblast differentiation but also provide strong suggestive evidence that osteoblasts may be promising targets in preventive and therapeutic strategies for osteoporosis. |
format | Online Article Text |
id | pubmed-7905819 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | American Chemical Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-79058192021-02-26 Cyanidin-3-glucoside Regulates Osteoblast Differentiation via the ERK1/2 Signaling Pathway Hu, Bosen Chen, Lin Chen, Yong Zhang, Zhuo Wang, Xiaohong Zhou, Bo ACS Omega [Image: see text] Osteoporosis, characterized by a gradual decrease in the number of osteoblasts and a gradual increase in bone resorption of osteoclasts in bone tissue, is a global chronic disease, which severely impairs the quality of life of the elderly. Therefore, it is extremely urgent to study the prevention and treatment of osteoporosis. It has been reported that anthocyanins can regulate bone metabolism and prevent osteoporosis. Cyanidin-3-O-glucoside (C3G), the most common type of anthocyanin in nature, widely exists in a variety of vegetables and fruits. Although it has been shown that C3G has multiple effects on osteoclasts, its impact(s) and underlying mechanism(s) on osteoblasts are still not clear. Here, we evaluated the effect of C3G on cell proliferation and differentiation of osteoblasts (extracted from the hip joint of patients with osteoporosis) and MC3T3-E1 (a kind of osteoblast cell line from mice). We also test the ability of osteoblasts to mineralize after C3G treatment. To find the underlying mechanism of the above effects, we further evaluated the role of the ERK signaling pathway in C3G regulation of osteoblasts. The results showed that C3G treatment enhanced osteoblast proliferation rate, osteoblast mineralization points, the mRNA levels and protein expression levels of OC (osteocalcin), and the level of ERK phosphorylation, which could be blocked by pretreatment with ERK signaling pathway inhibitor. The above results not only indicate that the ERK pathway was involved in C3G regulation of osteoblast differentiation but also provide strong suggestive evidence that osteoblasts may be promising targets in preventive and therapeutic strategies for osteoporosis. American Chemical Society 2021-02-11 /pmc/articles/PMC7905819/ /pubmed/33644583 http://dx.doi.org/10.1021/acsomega.0c05603 Text en © 2021 The Authors. Published by American Chemical Society Permits non-commercial access and re-use, provided that author attribution and integrity are maintained; but does not permit creation of adaptations or other derivative works (https://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Hu, Bosen Chen, Lin Chen, Yong Zhang, Zhuo Wang, Xiaohong Zhou, Bo Cyanidin-3-glucoside Regulates Osteoblast Differentiation via the ERK1/2 Signaling Pathway |
title | Cyanidin-3-glucoside Regulates Osteoblast Differentiation
via the ERK1/2 Signaling Pathway |
title_full | Cyanidin-3-glucoside Regulates Osteoblast Differentiation
via the ERK1/2 Signaling Pathway |
title_fullStr | Cyanidin-3-glucoside Regulates Osteoblast Differentiation
via the ERK1/2 Signaling Pathway |
title_full_unstemmed | Cyanidin-3-glucoside Regulates Osteoblast Differentiation
via the ERK1/2 Signaling Pathway |
title_short | Cyanidin-3-glucoside Regulates Osteoblast Differentiation
via the ERK1/2 Signaling Pathway |
title_sort | cyanidin-3-glucoside regulates osteoblast differentiation
via the erk1/2 signaling pathway |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905819/ https://www.ncbi.nlm.nih.gov/pubmed/33644583 http://dx.doi.org/10.1021/acsomega.0c05603 |
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