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Tripterygium glycosides inhibit inflammatory mediators in the rat synovial RSC-364 cell line stimulated with interleukin-1β

机译:雷公藤多甙抑制白介素-1β刺激的大鼠滑膜RSC-364细胞系中的炎性介质

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摘要

Tripterygium glycosides (TG) are extracted from a traditional Chinese medicinal herb. Using the compound, progress has been made in the treatment of rheumatoid arthritis (RA), but the underlying mechanism of its action is poorly understood. The purpose of the present study was to investigate the role of TG in preventing inflammatory arthritis. An inflammatory cell model was established in the rat synovial RSC-364 cell line via induction with interleukin (IL)-1β. The expression of IL-32 and matrix metalloproteinases (MMP-1 and MMP-9) was determined using an enzyme-linked immunosorbent assay. Compared with the control group (without IL-1β), IL-1β in the treatment group induced the expression of IL-32, MMP-1 and MMP-9 in RSC-364 cells. When a different dose of TG was added to RSC-364 cells stimulated with IL-1β, TG decreased the expression levels of IL-32, MMP-1 and MMP-9 in a dose-dependent manner. These results indicated that TG suppressed the inflammation response in RSC-364 cells. Taken together, these findings may contribute to a better understanding of the role of TG in the anti-inflammatory therapeutics for RA.
机译:雷公藤多甙(TG)提取自传统中草药。使用该化合物,在类风湿性关节炎(RA)的治疗方面已取得进展,但对其作用的潜在机制了解甚少。本研究的目的是研究TG在预防炎性关节炎中的作用。通过白介素(IL)-1β诱导在大鼠滑膜RSC-364细胞系中建立炎性细胞模型。使用酶联免疫吸附测定法测定IL-32和基质金属蛋白酶(MMP-1和MMP-9)的表达。与对照组(无IL-1β)相比,治疗组IL-1β诱导RSC-364细胞中IL-32,MMP-1和MMP-9的表达。当向IL-1β刺激的RSC-364细胞中加入不同剂量的TG时,TG以剂量依赖的方式降低IL-32,MMP-1和MMP-9的表达水平。这些结果表明TG抑制了RSC-364细胞中的炎症反应。综上所述,这些发现可能有助于更好地了解TG在RA抗炎治疗剂中的作用。

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