化学
肿瘤坏死因子α
TLR4型
炎症
蛋白激酶B
成纤维细胞
细胞因子
类风湿性关节炎
NF-κB
受体
信号转导
癌症研究
免疫学
医学
生物化学
体外
作者
Lingli Kong,Laifang Wang,Qing Zhao,Guijuan Di,Huiqiang Wu
摘要
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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