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Rhodojaponin II inhibits TNF-α-induced inflammatory cytokine secretion in MH7A human rheumatoid arthritis fibroblast-like synoviocytes.

Abstract
Rhodojaponin II (R-II) has been shown to possess anti-inflammatory activity. Herein, we aimed to explore the effect of R-II on tumor necrosis factor-α (TNF-α)-induced inflammation in MH7A rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLSs). We found that R-II treatment at high concentration suppressed the viability of MH7A cells. R-II suppressed the levels of nitric oxide and prostaglandin E2, and inhibited messenger RNA expression and concentrations of interleukin-1β (IL-1β), IL-6 and matrix metalloproteinase-1 in TNF-α-stimulated RA-FLSs. Additionally, R-II repressed TNF-α-induced activation of the Akt, nuclear factor-κB (NF-κB), and toll-like receptor 4 (TLR4)/MyD88 pathways in MH7A cells. Inhibition of the Akt, NF-κB, and TLR4/MyD88 pathways by the corresponding inhibitors reinforced the inhibitory effect of R-II on TNF-α-induced inflammatory cytokine secretion in MH7A cells. R-II ameliorated the severity of collagen-induced arthritis in mice by inhibiting inflammation. In conclusion, R-II repressed TNF-α-induced inflammatory response in MH7A cells by inactivating the Akt, NF-κB, and TLR4/MyD88 pathways.
AuthorsLingli Kong, Laifang Wang, Qing Zhao, Guijuan Di, Huiqiang Wu
JournalJournal of biochemical and molecular toxicology (J Biochem Mol Toxicol) Vol. 34 Issue 10 Pg. e22551 (Oct 2020) ISSN: 1099-0461 [Electronic] United States
PMID32613688 (Publication Type: Journal Article)
Copyright© 2020 Wiley Periodicals LLC.
Chemical References
  • Cytokines
  • Diterpenes
  • Inflammation Mediators
  • Tumor Necrosis Factor-alpha
  • rhodojaponin II
Topics
  • Arthritis, Rheumatoid (metabolism, pathology)
  • Cell Line
  • Cytokines (metabolism)
  • Diterpenes (pharmacology)
  • Enzyme-Linked Immunosorbent Assay
  • Fibroblasts (metabolism, pathology)
  • Humans
  • Inflammation Mediators (metabolism)
  • Real-Time Polymerase Chain Reaction
  • Synoviocytes (metabolism, pathology)
  • Tumor Necrosis Factor-alpha (antagonists & inhibitors)

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