Journal
CHEMICO-BIOLOGICAL INTERACTIONS
Volume 258, Issue -, Pages 175-186Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2016.09.003
Keywords
Rheumatoid arthritis; Trikatu; Fibroblast-like synoviocytes; Inflammatory mediators; IL-17; NF kappa B
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The present study was designed to investigate the potential therapeutic effect of trikatu, an herbal compound and its underlying molecular mechanism in rats with adjuvant-induced arthritis (AIA). Our results indicate that trikatu (1000 mg/kg/b.wt. oral) administration suppressed the production of proinflammatory cytokines (tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, IL-6, and monocyte chemoattractant protein (MCP)-1) and downregulated the mRNA expression levels of inflammatory mediators (TNF-alpha, IL-1 beta, IL-6, IL-17, MCP-1, receptor activator of nuclear factor kappa B ligand (RANKL), cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS)) and transcription factors (nuclear factor kappa B 65 (NF kappa B-p65) and activator protein-1 (AP-1)) in cultured AIA-fibroblast like synoviocytes and synovial tissue of AIA rats. Consistently, the protein expression of NF kappa B-p65, IL-17, TNF-alpha, COX-2, and RANKL was also dramatically reduced in cultured AIA-fibroblast like synoviocytes and synovial tissue of AIA rats by trikatu treatment. In addition, trikatu suppressed the expression and phosphorylation of NF kappa B-p65 similar to the Bay 11-7082 (NF kappa B inhibitor) in cultured AIA-fibroblast like synoviocytes. Furthermore, trikatu alleviated the histopathology of joint of arthritic rats. Overall, these data highlights that trikatu could be a promising alternative modality for the possible treatment of rheumatoid arthritis and other inflammatory diseases. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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