首页> 外文期刊>Journal of biochemical and molecular toxicology >Rhodojaponin II inhibits TNF-α-induced inflammatory cytokine secretion in MH7A human rheumatoid arthritis fibroblast-like synoviocytes
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Rhodojaponin II inhibits TNF-α-induced inflammatory cytokine secretion in MH7A human rheumatoid arthritis fibroblast-like synoviocytes

机译:rhodojaponin II抑制MH7A人类风湿性关节炎成纤维细胞样Synociytes中的TNF-α诱导的炎症细胞因子分泌物

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Rhodojaponin II (R-II) has been shown to possess anti-inflammatory activity. Herein, we aimed to explore the effect of R-ll on tumor necrosis factor-α (TNF-α)-induced inflammation in MH7A rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLSs). We found that R-ll treatment at high concentration suppressed the viability of MH7A cells. R-ll 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-ll 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-ll on TNF-α-induced inflammatory cytokine secretion in MH7A cells. R-ll ameliorated the severity of collagen-induced arthritis in mice by inhibiting inflammation. In conclusion, R-ll repressed TNF-α-induced inflammatory response in MH7A cells by inactivating the Akt, NF-κB, and TLR4/MyD88 pathways.
机译:Rhodojaponin II(R-II)已被证明具有抗炎活性。在此,我们旨在探讨R-ll对肿瘤坏死因子-α(TNF-α)诱导的MH7A类风湿性关节炎(RA)成纤维细胞样滑膜细胞(FLS)炎症的影响。我们发现高浓度的R-ll处理抑制了MH7A细胞的活力。在TNF-α刺激的RA FLSs中,R-ll抑制一氧化氮和前列腺素E2的水平,抑制信使RNA的表达和白细胞介素-1β(IL-1β)、白细胞介素-6和基质金属蛋白酶-1的浓度。此外,在MH7A细胞中,R-ll抑制TNF-α诱导的Akt、核因子-κB(NF-κB)和toll样受体4(TLR4)/MyD88通路的激活。相应抑制剂对Akt、NF-κB和TLR4/MyD88通路的抑制增强了R-ll对MH7A细胞中TNF-α诱导的炎性细胞因子分泌的抑制作用。R-ll通过抑制炎症改善小鼠胶原诱导的关节炎的严重程度。总之,R-ll通过使Akt、NF-κB和TLR4/MyD88通路失活来抑制MH7A细胞中TNF-α诱导的炎症反应。

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