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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：Doliroside A通过靶向NLRP3炎症小体减轻尿酸单钠晶体诱导的炎症

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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：我们先前的研究表明，Dolichos Maim Klein（DU）可以改善尿酸单钠（MSU）晶体诱发的痛风性关节炎，而根据体外研究，其中的一种有效成分多洛洛糖苷A有助于OF的抗痛风性关节炎作用。但是，关于多洛洛糖苷A对痛风性关节炎的潜在有益作用和可能的作用机理，人们仍知之甚少。在这里，我们调查了多洛西苷A在体外的潜在作用机理以及多洛西苷A在体内的抗炎作用。在脂多糖（LPS）之前或之后，用多洛伊糖苷A处理源自骨髓的巨噬细胞，然后用MSU晶体，尼日利亚霉素和三磷酸腺苷（ATP）刺激。分析了与激活核苷酸结合结构域和富含亮氨酸重复序列的蛋白3（NLRP3）炎性小体相关的蛋白表达。结果表明，多洛洛糖苷A（15、30、45和60μM）抑制LPS诱导的巨噬细胞引发和炎症小体活化。此外，向用MSU晶体治疗的大鼠施用多洛洛糖苷A。结果表明，多洛洛糖苷A（10、20和40 mg / 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-1 beta（pro-IL- MSU晶体处理大鼠中的1 beta）蛋白。这些发现表明，多洛洛糖苷A对缓解由MSU晶体引起的痛风性关节炎具有显著作用。多洛洛糖苷A对痛风性关节炎的作用是通过影响LPS诱导的引发和炎症小体的激活来抑制caspase-1和IL-1β分泌的激活而发挥的。 （C）2014 Elsevier B.V.保留所有权利。

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