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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Doliroside A attenuates monosodium urate crystals-induced inflammation by targeting NLRP3 inflammasome
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Doliroside A attenuates monosodium urate crystals-induced inflammation by targeting NLRP3 inflammasome

机译：通过靶向NLRP3炎性炎症剂A衰减单钠尿液晶体诱导的炎症

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摘要

Our previous study demonstrates that Dolichos Maim Klein (DU) ameliorates the gouty arthritis induced by monosodium urate (MSU) crystals, and one of the active components, doliroside A, contributed to the antigouty arthritis effect of OF according to the in vitro study. However, there is still little known about the potential beneficial effects and possible mechanism of action of doliroside A on gouty arthritis. Here, we investigated the underlying mechanism of action of doliroside A in vitro and the anti-inflammatory effects of doliroside A in vivo. Bone-marrow-derived macrophages were treated with doliroside A before or after lipopolysaccharide (LPS) and then stimulated with MSU crystals, nigericin and adenosine triphosphate (ATP). The expressions of proteins related to activation of nucleotide-binding domain and leucine-rich repeat containing protein 3 (NLRP3) inflammasome were analyzed. The results manifested that doliroside A (15, 30, 45 and 60 mu M) suppressed both LPS-induced priming and inflammasome activation in macrophages. Moreover, doliroside A was administered to the rats treated by MSU crystals. The results demonstrated that doliroside A (10, 20 and 40 mg/kg) ameliorated the symptoms of gouty arthritis, decreased the levels of proinflammatory cytokines, and inhibited the expressions of caspase-1 and pro-interleukin-1 beta (pro-IL-1 beta) proteins in MSU crystals-treated rats. These findings indicate that doliroside A exhibits a prominent effect on ameliorating gouty arthritis induced by MSU crystals. The action of doliroside A on gouty arthritis exerts via inhibiting the activation of caspase-1 and IL-1 beta secretion by affecting both LPS-induced priming and inflammasome activation. (C) 2014 Elsevier B.V. All rights reserved.
机译：我们以前的研究表明，Dolichos Maim Klein（DU）改善了由单钠（MSU）晶体（MSU）晶体诱导的痛风性关节炎，以及其中一种活性组分Doloroside A，导致根据体外研究的抗原性关节炎效应。然而，仍然对多血清虫A对痛风性关节炎的潜在有益效果和可能的作用机制毫无熟悉。在这里，我们调查了多血清藻酰胺的潜在机制和体内二硫代罗酯A的抗炎作用。骨髓衍生的巨噬细胞用脂多糖（LPS）之前或之后用Doliroside A处理，然后用MSU晶体，Nigericin和三磷酸腺苷（ATP）刺激。分析了与核苷酸结合结构域和富含亮氨酸富含含蛋白3（NLRP3）炎症的激活相关的蛋白质的表达。结果表明，二硼化吡硼吡啶A（15,30,45和60μm）抑制了巨噬细胞中的LPS诱导的灌注和炎症组活化。此外，将多硅烷A施用于由MSU晶体处理的大鼠。结果表明，二硼化吡吡硼吡硼（10,20和40mg / kg）改善了痛风性关节炎的症状，降低了促炎细胞因子的水平，并抑制了Caspase-1和Pro-Interleukin-1β的表达（Pro-IL- MSU晶体处理大鼠中的1个β）蛋白。这些发现表明，Doliroside A对改善MSU晶体诱导的痛风性关节炎表现出突出的影响。二硼化钠A对痛风性关节炎的作用通过抑制Caspase-1和IL-1β分泌通过影响LPS诱导的引发和炎症体活化来施加活化。 （c）2014 Elsevier B.V.保留所有权利。

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