ArticleArthritis and rheumatism2013
Sulforaphane represses matrix-degrading proteases and protects cartilage from destruction in vitro and in vivo.
Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 80 citations in OpenAlex.
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- Article
- GSH Levels Serve As a Biological Redox Switch Regulating Sulforaphane-Induced Cell Fate in Human Lens Cells.Investigative ophthalmology & visual science · 2021Article
- Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis.Molecular medicine reports · 2021Article
- Article
- Intersections Between Mitochondrial Metabolism and Redox Biology Mediate Posttraumatic Osteoarthritis.Current rheumatology reports · 2021Review
- Pharmacological Targeting of Heme Oxygenase-1 in Osteoarthritis.Antioxidants (Basel, Switzerland) · 2021Review
- Effect of interleukin-6, -17, -21, -22, and -23 and STAT3 on signal transduction pathways and their inhibition in autoimmune arthritis.Immunologic research · 2021Review
- Experimental Therapeutics for the Treatment of Osteoarthritis.Journal of experimental pharmacology · 2021Review
- Therapeutic Potential of Bioactive Compounds in Honey for Treating Osteoarthritis.Frontiers in pharmacology · 2021Review
- The role of microRNA-3085 in chondrocyte function.Scientific reports · 2020Article
- Role of iNOS in osteoarthritis: Pathological and therapeutic aspects.Journal of cellular physiology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveSulforaphane (SFN) has been reported to regulate signaling pathways relevant to chronic diseases. The aim of this study was to investigate the impact of SFN treatment on signaling pathways in chondrocytes and to determine whether sulforaphane could block cartilage destruction in osteoarthritis.
methodsGene expression, histone acetylation, and signaling of the transcription factors NF-E2-related factor 2 (Nrf2) and NF-κB were examined in vitro. The bovine nasal cartilage explant model and the destabilization of the medial meniscus (DMM) model of osteoarthritis in the mouse were used to assess chondroprotection at the tissue and whole-animal levels.
resultsSFN inhibited cytokine-induced metalloproteinase expression in primary human articular chondrocytes and in fibroblast-like synovial cells. SFN acted independently of Nrf2 and histone deacetylase activity to regulate metalloproteinase expression in human articular chondrocytes but did mediate prolonged activation of JNK and p38 MAPK. SFN attenuated NF-κB signaling at least through inhibition of DNA binding in human articular chondrocytes, with decreased expression of several NF-κB-dependent genes. Compared with cytokines alone, SFN (10 μM) abrogated cytokine-induced destruction of bovine nasal cartilage at both the proteoglycan and collagen breakdown levels. An SFN-rich diet (3 μmoles/day SFN versus control chow) decreased the arthritis score in the DMM model of osteoarthritis in the mouse, with a concurrent block of early DMM-induced gene expression changes.
conclusionSFN inhibits the expression of key metalloproteinases implicated in osteoarthritis, independently of Nrf2, and blocks inflammation at the level of NF-κB to protect against cartilage destruction in vitro and in vivo.
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