Cargando…

Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL‐1β/NF‐κB pathway

The osteoarthritis (OA) progression is now considered to be related to inflammation. Anemonin (ANE) is a small natural molecule extracted from various kinds of Chinese traditional herbs and has been shown to inhibiting inflammation response. In this study, we examined whether ANE could attenuate the...

Descripción completa

Detalles Bibliográficos
Autores principales: Wang, Zuqiang, Huang, Junlan, Zhou, Siru, Luo, Fengtao, Xu, Wei, Wang, Quan, Tan, Qiaoyan, chen, Liang, Wang, Jun, Chen, Hangang, Chen, Lin, Xie, Yangli, Du, Xiaolan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706500/
https://www.ncbi.nlm.nih.gov/pubmed/28643466
http://dx.doi.org/10.1111/jcmm.13227
_version_ 1783282241522106368
author Wang, Zuqiang
Huang, Junlan
Zhou, Siru
Luo, Fengtao
Xu, Wei
Wang, Quan
Tan, Qiaoyan
chen, Liang
Wang, Jun
Chen, Hangang
Chen, Lin
Xie, Yangli
Du, Xiaolan
author_facet Wang, Zuqiang
Huang, Junlan
Zhou, Siru
Luo, Fengtao
Xu, Wei
Wang, Quan
Tan, Qiaoyan
chen, Liang
Wang, Jun
Chen, Hangang
Chen, Lin
Xie, Yangli
Du, Xiaolan
author_sort Wang, Zuqiang
collection PubMed
description The osteoarthritis (OA) progression is now considered to be related to inflammation. Anemonin (ANE) is a small natural molecule extracted from various kinds of Chinese traditional herbs and has been shown to inhibiting inflammation response. In this study, we examined whether ANE could attenuate the progression of OA via suppression of IL‐1β/NF‐κB pathway activation. Destabilization of the medial meniscus (DMM) was performed in 10‐week‐old male C57BL/6J mice. ANE was then intra‐articularly injected into joint capsule for 8 and 12 weeks. Human articular chondrocytes and cartilage explants challenged with interleukin‐1β (IL‐1β) were treated with ANE. We found that ANE delayed articular cartilage degeneration in vitro and in vivo. In particular, proteoglycan loss and chondrocyte hypertrophy were significantly decreased in ANE ‐treated mice compared with vehicle‐treated mice. ANE decreased the expressions of matrix metalloproteinase‐13 (MMP13), A disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5), collagen X (Col X) while increasing Aggrecan level in murine with DMM surgery. ANE treatment also attenuated proteoglycan loss in human cartilage explants treated with IL‐1β ex vivo. ANE is a potent protective molecule for OA; it delays OA progression by suppressing ECM loss and chondrocyte hypertrophy partially by suppressing IL‐1β/NF‐κB pathway activation.
format Online
Article
Text
id pubmed-5706500
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-57065002017-12-06 Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL‐1β/NF‐κB pathway Wang, Zuqiang Huang, Junlan Zhou, Siru Luo, Fengtao Xu, Wei Wang, Quan Tan, Qiaoyan chen, Liang Wang, Jun Chen, Hangang Chen, Lin Xie, Yangli Du, Xiaolan J Cell Mol Med Original Articles The osteoarthritis (OA) progression is now considered to be related to inflammation. Anemonin (ANE) is a small natural molecule extracted from various kinds of Chinese traditional herbs and has been shown to inhibiting inflammation response. In this study, we examined whether ANE could attenuate the progression of OA via suppression of IL‐1β/NF‐κB pathway activation. Destabilization of the medial meniscus (DMM) was performed in 10‐week‐old male C57BL/6J mice. ANE was then intra‐articularly injected into joint capsule for 8 and 12 weeks. Human articular chondrocytes and cartilage explants challenged with interleukin‐1β (IL‐1β) were treated with ANE. We found that ANE delayed articular cartilage degeneration in vitro and in vivo. In particular, proteoglycan loss and chondrocyte hypertrophy were significantly decreased in ANE ‐treated mice compared with vehicle‐treated mice. ANE decreased the expressions of matrix metalloproteinase‐13 (MMP13), A disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5), collagen X (Col X) while increasing Aggrecan level in murine with DMM surgery. ANE treatment also attenuated proteoglycan loss in human cartilage explants treated with IL‐1β ex vivo. ANE is a potent protective molecule for OA; it delays OA progression by suppressing ECM loss and chondrocyte hypertrophy partially by suppressing IL‐1β/NF‐κB pathway activation. John Wiley and Sons Inc. 2017-06-23 2017-12 /pmc/articles/PMC5706500/ /pubmed/28643466 http://dx.doi.org/10.1111/jcmm.13227 Text en © 2017 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 Creative Commons Attribution (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
Wang, Zuqiang
Huang, Junlan
Zhou, Siru
Luo, Fengtao
Xu, Wei
Wang, Quan
Tan, Qiaoyan
chen, Liang
Wang, Jun
Chen, Hangang
Chen, Lin
Xie, Yangli
Du, Xiaolan
Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL‐1β/NF‐κB pathway
title Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL‐1β/NF‐κB pathway
title_full Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL‐1β/NF‐κB pathway
title_fullStr Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL‐1β/NF‐κB pathway
title_full_unstemmed Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL‐1β/NF‐κB pathway
title_short Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL‐1β/NF‐κB pathway
title_sort anemonin attenuates osteoarthritis progression through inhibiting the activation of il‐1β/nf‐κb pathway
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706500/
https://www.ncbi.nlm.nih.gov/pubmed/28643466
http://dx.doi.org/10.1111/jcmm.13227
work_keys_str_mv AT wangzuqiang anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT huangjunlan anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT zhousiru anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT luofengtao anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT xuwei anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT wangquan anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT tanqiaoyan anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT chenliang anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT wangjun anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT chenhangang anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT chenlin anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT xieyangli anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway
AT duxiaolan anemoninattenuatesosteoarthritisprogressionthroughinhibitingtheactivationofil1bnfkbpathway