Cargando…

Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL‐induced osteoclastogenesis

Osteoporosis is the most common osteolytic disease characterized by excessive osteoclast formation and resultant bone loss, which afflicts millions of patients around the world. Astilbin, a traditional herb, is known to have anti‐inflammatory, antioxidant and antihepatic properties, but its role in...

Descripción completa

Detalles Bibliográficos
Autores principales: Jin, Haiming, Wang, Qingqing, Chen, Kai, Xu, Ke, Pan, Hao, Chu, Feifan, Ye, Zhen, Wang, Ziyi, Tickner, Jennifer, Qiu, Heng, Wang, Chao, Kenny, Jacob, Xu, Huazi, Wang, Te, Xu, Jiake
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850941/
https://www.ncbi.nlm.nih.gov/pubmed/31603626
http://dx.doi.org/10.1111/jcmm.14713
_version_ 1783469537827487744
author Jin, Haiming
Wang, Qingqing
Chen, Kai
Xu, Ke
Pan, Hao
Chu, Feifan
Ye, Zhen
Wang, Ziyi
Tickner, Jennifer
Qiu, Heng
Wang, Chao
Kenny, Jacob
Xu, Huazi
Wang, Te
Xu, Jiake
author_facet Jin, Haiming
Wang, Qingqing
Chen, Kai
Xu, Ke
Pan, Hao
Chu, Feifan
Ye, Zhen
Wang, Ziyi
Tickner, Jennifer
Qiu, Heng
Wang, Chao
Kenny, Jacob
Xu, Huazi
Wang, Te
Xu, Jiake
author_sort Jin, Haiming
collection PubMed
description Osteoporosis is the most common osteolytic disease characterized by excessive osteoclast formation and resultant bone loss, which afflicts millions of patients around the world. Astilbin, a traditional herb, is known to have anti‐inflammatory, antioxidant and antihepatic properties, but its role in osteoporosis treatment has not yet been confirmed. In our study, astilbin was found to have an inhibitory effect on the RANKL‐induced formation and function of OCs in a dose‐dependent manner without cytotoxicity. These effects were attributed to its ability to suppress the activity of two transcription factors (NFATc1 and c‐Fos) indispensable for osteoclast formation, followed by inhibition of the expression of bone resorption‐related genes and proteins (Acp5/TRAcP, CTSK, V‐ATPase‐d2 and integrin β3). Furthermore, we examined the underlying mechanisms and found that astilbin repressed osteoclastogenesis by blocking Ca(2+) oscillations and the NF‐κB and MAPK pathways. In addition, the therapeutic effect of MA on preventing bone loss in vivo was further confirmed in an ovariectomized mouse model. Therefore, considering its ability to inhibit RANKL‐mediated osteoclastogenesis and the underlying mechanisms, astilbin might be a potential candidate for treating osteolytic bone diseases.
format Online
Article
Text
id pubmed-6850941
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-68509412019-12-01 Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL‐induced osteoclastogenesis Jin, Haiming Wang, Qingqing Chen, Kai Xu, Ke Pan, Hao Chu, Feifan Ye, Zhen Wang, Ziyi Tickner, Jennifer Qiu, Heng Wang, Chao Kenny, Jacob Xu, Huazi Wang, Te Xu, Jiake J Cell Mol Med Original Articles Osteoporosis is the most common osteolytic disease characterized by excessive osteoclast formation and resultant bone loss, which afflicts millions of patients around the world. Astilbin, a traditional herb, is known to have anti‐inflammatory, antioxidant and antihepatic properties, but its role in osteoporosis treatment has not yet been confirmed. In our study, astilbin was found to have an inhibitory effect on the RANKL‐induced formation and function of OCs in a dose‐dependent manner without cytotoxicity. These effects were attributed to its ability to suppress the activity of two transcription factors (NFATc1 and c‐Fos) indispensable for osteoclast formation, followed by inhibition of the expression of bone resorption‐related genes and proteins (Acp5/TRAcP, CTSK, V‐ATPase‐d2 and integrin β3). Furthermore, we examined the underlying mechanisms and found that astilbin repressed osteoclastogenesis by blocking Ca(2+) oscillations and the NF‐κB and MAPK pathways. In addition, the therapeutic effect of MA on preventing bone loss in vivo was further confirmed in an ovariectomized mouse model. Therefore, considering its ability to inhibit RANKL‐mediated osteoclastogenesis and the underlying mechanisms, astilbin might be a potential candidate for treating osteolytic bone diseases. John Wiley and Sons Inc. 2019-10-11 2019-12 /pmc/articles/PMC6850941/ /pubmed/31603626 http://dx.doi.org/10.1111/jcmm.14713 Text en © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Jin, Haiming
Wang, Qingqing
Chen, Kai
Xu, Ke
Pan, Hao
Chu, Feifan
Ye, Zhen
Wang, Ziyi
Tickner, Jennifer
Qiu, Heng
Wang, Chao
Kenny, Jacob
Xu, Huazi
Wang, Te
Xu, Jiake
Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL‐induced osteoclastogenesis
title Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL‐induced osteoclastogenesis
title_full Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL‐induced osteoclastogenesis
title_fullStr Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL‐induced osteoclastogenesis
title_full_unstemmed Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL‐induced osteoclastogenesis
title_short Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL‐induced osteoclastogenesis
title_sort astilbin prevents bone loss in ovariectomized mice through the inhibition of rankl‐induced osteoclastogenesis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850941/
https://www.ncbi.nlm.nih.gov/pubmed/31603626
http://dx.doi.org/10.1111/jcmm.14713
work_keys_str_mv AT jinhaiming astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT wangqingqing astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT chenkai astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT xuke astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT panhao astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT chufeifan astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT yezhen astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT wangziyi astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT ticknerjennifer astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT qiuheng astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT wangchao astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT kennyjacob astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT xuhuazi astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT wangte astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis
AT xujiake astilbinpreventsbonelossinovariectomizedmicethroughtheinhibitionofranklinducedosteoclastogenesis