Open AccessAnemonin attenuates osteoarthritis progression through inhibiting the activation of IL ‐1β/ NF ‐κB pathway
Author(s) -
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
Publication year - 2017
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13227
Subject(s) - aggrecan , osteoarthritis , thrombospondin , adamts , inflammation , matrix metalloproteinase , cartilage , metalloproteinase , chemistry , chondrocyte , in vivo , proteoglycan , ex vivo , microbiology and biotechnology , medicine , in vitro , immunology , pathology , anatomy , biology , biochemistry , articular cartilage , alternative medicine
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 C57 BL /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 ( MMP 13), A disintegrin and metalloproteinase with thrombospondin motifs 5 ( ADAMTS 5), 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.