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Erschienen in: Inflammation 4/2017

31.03.2017 | ORIGINAL ARTICLE

Chrysin Attenuates IL-1β-Induced Expression of Inflammatory Mediators by Suppressing NF-κB in Human Osteoarthritis Chondrocytes

verfasst von: Wenhao Zheng, Zhenyu Tao, Leyi Cai, Chunhui Chen, Chuanxu Zhang, Quan Wang, Xiaozhou Ying, Wei Hu, Hua Chen

Erschienen in: Inflammation | Ausgabe 4/2017

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Abstract

Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage degradation and inflammation. Chrysin, a natural flavonoid extracted from honey and propolis, has been reported to have anti-inflammatory effects. However, the anti-inflammatory effects of chrysin on OA have not been reported. This study aimed to assess the effects of chrysin on human OA chondrocytes. Human OA chondrocytes were pretreated with chrysin (1, 5, 10 μM) for 2 h and subsequently stimulated with IL-1β for 24 h. Production of NO, PGE2, MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 was evaluated by the Griess reaction and ELISAs. The messenger RNA (mRNA) expression of COX-2, iNOS, MMP-1, MMP-3, MMP-13, ADAMTS-4, ADAMTS-5, aggrecan, and collagen-II was measured by real-time PCR. The protein expression of COX-2, iNOS, p65, p-p65, IκB-α, and p-IκB-α was detected by Western blot. The protein expression of collagen-II and p65 nuclear translocation was evaluated by immunofluorescence. We found that chrysin significantly inhibited the IL-1β-induced production of NO and PGE2; expression of COX-2, iNOS, MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5; and degradation of aggrecan and collagen-II. Furthermore, chrysin dramatically blocked IL-1β-stimulated IκB-α degradation and NF-κB activation. Taken together, these results suggest that chrysin may be a potential agent in the treatment of OA.
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Metadaten
Titel
Chrysin Attenuates IL-1β-Induced Expression of Inflammatory Mediators by Suppressing NF-κB in Human Osteoarthritis Chondrocytes
verfasst von
Wenhao Zheng
Zhenyu Tao
Leyi Cai
Chunhui Chen
Chuanxu Zhang
Quan Wang
Xiaozhou Ying
Wei Hu
Hua Chen
Publikationsdatum
31.03.2017
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 4/2017
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-017-0558-9

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