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Garcinol Suppresses IL-1β-Induced Chondrocyte Inflammation and Osteoarthritis via Inhibition of the NF-κB Signaling Pathway.
- Source :
-
Inflammation [Inflammation] 2019 Oct; Vol. 42 (5), pp. 1754-1766. - Publication Year :
- 2019
-
Abstract
- Osteoarthritis (OA), which is characterized as a common degenerative joint disease, is presently the most prevalent chronic degenerative joint disease. Accumulating evidence has shown a biological function for Garcinol in a variety of diseases; however, whether it could be used to treat OA remains unclear. In this study, we explored the protective effects of garcinol on the progression of OA and explored the underlying mechanism. In vitro, garcinol reduced the expression of pro-inflammatory cytokines, such as IL-6 and tumor necrosis factor alpha (TNF-α). It also decreased the expression of inducible nitric oxide synthase (iNOS), as well as cyclooxygenase-2 (COX-2). Furthermore, garcinol inhibited the expression of thrombospondin motifs 5(ADAMTS5) and metalloproteinase (MMPs), both of which regulate extracellular matrix degradation. These changes could be attributed to garcinol-related suppression of the IL-1β-induced NF-κB signaling pathway. Moreover, we investigated the protective effects of garcinol on the surgical destabilization of the medial meniscus (DMM) of the mouse, an in vivo model of OA. Taken together, our data suggest garcinol as a potential future agent for the treatment of OA.
- Subjects :
- Animals
Cells, Cultured
Cyclooxygenase 2 metabolism
Cytokines metabolism
Humans
Inflammation chemically induced
Interleukin-1beta pharmacology
Mice
Nitric Oxide Synthase Type II metabolism
Osteoarthritis metabolism
Signal Transduction drug effects
Terpenes therapeutic use
Chondrocytes pathology
Inflammation prevention & control
NF-kappa B antagonists & inhibitors
Osteoarthritis prevention & control
Terpenes pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1573-2576
- Volume :
- 42
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Inflammation
- Publication Type :
- Academic Journal
- Accession number :
- 31201586
- Full Text :
- https://doi.org/10.1007/s10753-019-01037-7