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- Title
Formononetin Antagonizes the Interleukin-1β-Induced Catabolic Effects Through Suppressing Inflammation in Primary Rat Chondrocytes.
- Authors
Cho, In-A; Kim, Tae-Hyeon; Lim, HyangI; Park, Jong-Hyun; Kang, Kyeong-Rok; Lee, Sook-Young; Kim, Chun Sung; Kim, Do Kyung; Kim, Heung-Joong; Yu, Sun-Kyoung; Kim, Su-Gwan; Kim, Jae-Sung
- Abstract
In the present study, we demonstrated the anti-catabolic effects of formononetin, a phytoestrogen derived from herbal plants, against interleukin-1β (IL-1β)-induced severe catabolic effects in primary rat chondrocytes and articular cartilage. Formononetin did not affect the viability of primary rat chondrocytes in both short- (24 h) and long-term (21 days) treatment periods. Furthermore, formononetin effectively antagonized the IL-1β-induced catabolic effects including the decrease in proteoglycan content, suppression of pericellular matrix formation, and loss of proteoglycan through the decreased expression of cartilage-degrading enzymes like matrix metalloproteinase (MMP)-13, MMP-1, and MMP-3 in primary rat chondrocytes. Moreover, catabolic oxidative stress mediators like nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, and prostaglandin E2 were significantly downregulated by formononetin in primary rat chondrocytes treated with IL-1β. Sequentially, the upregulation of pro-inflammatory cytokines (like IL-1α, IL-1β, IL-6, and tumor necrosis factor α), chemokines (like fractalkine, monocyte chemoattractant protein-1, and macrophage inflammatory protein-3α), and vascular endothelial growth factor were significantly downregulated by formononetin in primary rat chondrocytes treated with IL-1β. These data suggest that formononetin may suppress IL-1β-induced severe catabolic effects and osteoarthritic condition. Furthermore, formononetin may be a promising candidate for the treatment and prevention of osteoarthritis.
- Subjects
VASCULAR endothelial growth factors; FORMONONETIN; CARTILAGE cells; TUMOR necrosis factors; NITRIC-oxide synthases
- Publication
Inflammation, 2019, Vol 42, Issue 4, p1426
- ISSN
0360-3997
- Publication type
Article
- DOI
10.1007/s10753-019-01005-1