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.
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Authors | Lingli Kong, Laifang Wang, Qing Zhao, Guijuan Di, Huiqiang Wu |
Journal | Journal of biochemical and molecular toxicology
(J Biochem Mol Toxicol)
Vol. 34
Issue 10
Pg. e22551
(Oct 2020)
ISSN: 1099-0461 [Electronic] United States |
PMID | 32613688
(Publication Type: Journal Article)
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Copyright | © 2020 Wiley Periodicals LLC. |
Chemical References |
- Cytokines
- Diterpenes
- Inflammation Mediators
- Tumor Necrosis Factor-alpha
- rhodojaponin II
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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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