首页> 美国卫生研究院文献>BioMed Research International >1,25-Dihydroxyvitamin D3 Inhibits the RANKL Pathway and Impacts on the Production of Pathway-Associated Cytokines in Early Rheumatoid Arthritis
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1,25-Dihydroxyvitamin D3 Inhibits the RANKL Pathway and Impacts on the Production of Pathway-Associated Cytokines in Early Rheumatoid Arthritis

机译:1,25-二羟基维生素D3抑制类风湿关节炎早期RANKL通路及其对通路相关细胞因子产生的影响

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摘要

Objectives. To study effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on RANKL signaling pathway and pathway-associated cytokines in patients with rheumatoid arthritis (RA). Methods. Receptor activator of nuclear factor-kappa B ligand (RANKL), osteoprotegerin (OPG), IFN-γ, IL-6, TNF-α, IL-17, and IL-4 were examined in 54 patients with incipient RA using a cytometric bead array (CBA) or an enzyme-linked immunosorbent assay (ELISA). Results. After 72 hours of incubation of peripheral blood mononuclear cells (PBMCs) with 1,25(OH)2D3 in RA patients, the levels of RANKL, TNF-α, IL-17 and IL-6 significantly decreased compared to those of the control. 1,25(OH)2D3 had no significantly impact on the levels of OPG, RANKL/OPG, and IL-4. Conclusions. The present study demonstrated that 1,25(OH)2D3 reduced the production of RANKL and the secretion of TNF-α, IL-17, and IL-6 in PBMCs of RA patients, which indicated that 1,25(OH)2D3 might be able to decrease damage of cartilage and bone in RA patients by regulating the expression of RANKL signaling pathway and pathway-associated cytokines.
机译:目标。研究1,25-二羟基维生素D3(1,25(OH)2D3)对类风湿关节炎(RA)患者RANKL信号通路和通路相关细胞因子的影响。方法。使用细胞计数珠对54例初发RA患者进行了核因子-κB配体(RANKL),骨保护素(OPG),IFN-γ,IL-6,TNF-α,IL-17和IL-4受体激活剂的检测阵列(CBA)或酶联免疫吸附测定(ELISA)。结果。在RA患者中将外周血单核细胞(PBMC)与1,25(OH)2D3孵育72小时后,与对照组相比,RANKL,TNF-α,IL-17和IL-6的水平明显降低。 1,25(OH)2D3对OPG,RANKL / OPG和IL-4的水平无明显影响。结论。本研究表明1,25(OH)2D3减少了RA患者PBMC中RANKL的产生以及TNF-α,IL-17和IL-6的分泌,这表明1,25(OH)2D3可能通过调节RANKL信号通路和通路相关细胞因子的表达,能够减少RA患者的软骨和骨骼损伤。

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