Artikel
Antirheumatic effect of Sulforaphan
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Veröffentlicht: | 16. Oktober 2008 |
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Gliederung
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Objective: Rheumatoid arthritis (RA) is a chronic inflammatory disease in which the synovial environment is characterized by intense immunological activity. We investigated whether sulforaphane (SF) could inhibit the expression of interleukin 6 (IL-6), and IL-1 as well as cell proliferation induced by tumor necrosis factor-α (TNF α) in human immortalised fibroblast-like synoviocytes (FLS).
Methods: FLS were cultured with or without SF. Cytokine and VEGF secretion levels were detected using ELISA. Cell proliferation of FLS induced by TNF-α was determined by Cyquant. NFκB and AP-1 activity was measured by Dual-Luciferase-Assay.
Results: ELISA and promoter-studies analysis revealed that the activity of NFκB and AP-1 and the levels of IL-6, and IL-1 secretion by FLS were reduced by SF in a dose-dependent manner. Cyquant assay showed that SF could inhibit proliferation of FLS induced by TNF-α.
Conclusion: Our results demonstrate that SF inhibits “pro-inflammatory”- transcription factors and -cytokines in FLS. In addition, it reduces TNF-α induced FLS cell proliferation. These findings indicate that treatment of RA-patients with SF might be considered as a new therapeutic strategy to combat joint destruction and inflammation in RA.