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Alginate oligosaccharide alleviates senile osteoporosis via the RANKL–RANK pathway in D‐galactose‐induced C57BL/6J mice

Osteoporosis is a systemic skeletal disorder characterized by reduced bone mineral density (BMD) and bone quality and increased bone porosity, which increase the risk of bone fracture. Inflammation, one of the important mechanisms related to aging, is associated with osteoporosis. Treatment with ant...

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Autores principales: Wang, Shan, Feng, Wenjing, Liu, Jianya, Wang, Xufu, Zhong, Lina, Lv, Chengxiu, Feng, Meiping, An, Nina, Mao, Yongjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9544009/
https://www.ncbi.nlm.nih.gov/pubmed/34145772
http://dx.doi.org/10.1111/cbdd.13904
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author Wang, Shan
Feng, Wenjing
Liu, Jianya
Wang, Xufu
Zhong, Lina
Lv, Chengxiu
Feng, Meiping
An, Nina
Mao, Yongjun
author_facet Wang, Shan
Feng, Wenjing
Liu, Jianya
Wang, Xufu
Zhong, Lina
Lv, Chengxiu
Feng, Meiping
An, Nina
Mao, Yongjun
author_sort Wang, Shan
collection PubMed
description Osteoporosis is a systemic skeletal disorder characterized by reduced bone mineral density (BMD) and bone quality and increased bone porosity, which increase the risk of bone fracture. Inflammation, one of the important mechanisms related to aging, is associated with osteoporosis. Treatment with anti‐inflammatory agents is effective for alleviating senile osteoporosis. Alginate oligosaccharide (AOS) can prevent and treat diseases related to inflammation, oxidative stress, and immunity. This study evaluates the effect of AOS on osteoporosis and investigates the underlying mechanism. Osteoporosis model was induced by D‐galactose (D‐gal) (200 mg kg(−1) day(−1)) for eight weeks. Three groups were administered via AOS (50, 100, and 150 mg kg(−1) day(−1)) for four weeks, while a control group received sterile water (5 ml kg(−1) day(−1)) for 8 weeks. The results showed that AOS improved bone density and bone microstructure in D‐gal‐induced osteoporosis mice. AOS inhibited osteoclast proliferation, probably through the suppression of receptor activator of nuclear factor‐kappa B ligand (RANKL)‐associated nuclear factor kappa B (NF‐κB) and c‐Fos signaling pathway. AOS also increased osteoprotegerin (OPG) expression and competitively inhibited the binding between RANK and RANKL in senile osteoporosis. Further, AOS decreased the secretion of serum osteocalcin and reduced bone conversion. Together, these results demonstrate the anti‐osteoporosis activity of AOS in mice with osteoporosis.
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spelling pubmed-95440092022-10-14 Alginate oligosaccharide alleviates senile osteoporosis via the RANKL–RANK pathway in D‐galactose‐induced C57BL/6J mice Wang, Shan Feng, Wenjing Liu, Jianya Wang, Xufu Zhong, Lina Lv, Chengxiu Feng, Meiping An, Nina Mao, Yongjun Chem Biol Drug Des Research Article Osteoporosis is a systemic skeletal disorder characterized by reduced bone mineral density (BMD) and bone quality and increased bone porosity, which increase the risk of bone fracture. Inflammation, one of the important mechanisms related to aging, is associated with osteoporosis. Treatment with anti‐inflammatory agents is effective for alleviating senile osteoporosis. Alginate oligosaccharide (AOS) can prevent and treat diseases related to inflammation, oxidative stress, and immunity. This study evaluates the effect of AOS on osteoporosis and investigates the underlying mechanism. Osteoporosis model was induced by D‐galactose (D‐gal) (200 mg kg(−1) day(−1)) for eight weeks. Three groups were administered via AOS (50, 100, and 150 mg kg(−1) day(−1)) for four weeks, while a control group received sterile water (5 ml kg(−1) day(−1)) for 8 weeks. The results showed that AOS improved bone density and bone microstructure in D‐gal‐induced osteoporosis mice. AOS inhibited osteoclast proliferation, probably through the suppression of receptor activator of nuclear factor‐kappa B ligand (RANKL)‐associated nuclear factor kappa B (NF‐κB) and c‐Fos signaling pathway. AOS also increased osteoprotegerin (OPG) expression and competitively inhibited the binding between RANK and RANKL in senile osteoporosis. Further, AOS decreased the secretion of serum osteocalcin and reduced bone conversion. Together, these results demonstrate the anti‐osteoporosis activity of AOS in mice with osteoporosis. John Wiley and Sons Inc. 2021-11-18 2022-01 /pmc/articles/PMC9544009/ /pubmed/34145772 http://dx.doi.org/10.1111/cbdd.13904 Text en © 2021 The Authors. Chemical Biology & Drug Design published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Wang, Shan
Feng, Wenjing
Liu, Jianya
Wang, Xufu
Zhong, Lina
Lv, Chengxiu
Feng, Meiping
An, Nina
Mao, Yongjun
Alginate oligosaccharide alleviates senile osteoporosis via the RANKL–RANK pathway in D‐galactose‐induced C57BL/6J mice
title Alginate oligosaccharide alleviates senile osteoporosis via the RANKL–RANK pathway in D‐galactose‐induced C57BL/6J mice
title_full Alginate oligosaccharide alleviates senile osteoporosis via the RANKL–RANK pathway in D‐galactose‐induced C57BL/6J mice
title_fullStr Alginate oligosaccharide alleviates senile osteoporosis via the RANKL–RANK pathway in D‐galactose‐induced C57BL/6J mice
title_full_unstemmed Alginate oligosaccharide alleviates senile osteoporosis via the RANKL–RANK pathway in D‐galactose‐induced C57BL/6J mice
title_short Alginate oligosaccharide alleviates senile osteoporosis via the RANKL–RANK pathway in D‐galactose‐induced C57BL/6J mice
title_sort alginate oligosaccharide alleviates senile osteoporosis via the rankl–rank pathway in d‐galactose‐induced c57bl/6j mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9544009/
https://www.ncbi.nlm.nih.gov/pubmed/34145772
http://dx.doi.org/10.1111/cbdd.13904
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