首页> 美国卫生研究院文献>Mediators of Inflammation >Anti-Inflammatory Effect of Rhapontici Radix Ethanol Extract via Inhibition of NF-κB and MAPK and Induction of HO-1 in Macrophages
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Anti-Inflammatory Effect of Rhapontici Radix Ethanol Extract via Inhibition of NF-κB and MAPK and Induction of HO-1 in Macrophages

机译:NF-κB和MAPK的抑制及HO-1在巨噬细胞中的诱导对拟南芥乙醇提取物的抗炎作用

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摘要

Rhapontici Radix (RR) has been used in traditional medicine in East Asia and has been shown to have various beneficial effects. However, its biological properties or mechanism on inflammation-related diseases is unknown. The goal of this study was to determine the anti-inflammatory activity and underlying molecular mechanisms of Rhapontici Radix ethanol extract (RRE). The inhibitory effect of RRE on the production of NO, cytokines, inflammatory-related proteins, and mRNAs in LPS-stimulated macrophages was determined by the Griess assay, ELISA, Western blot analysis, and real-time RT-PCR, respectively. Our results indicate that treatment with RRE significantly inhibited the secretion of NO and inflammatory cytokines in RAW 264.7 cells and mouse peritoneal macrophages without cytotoxicity. We also found that RRE strongly suppressed the expression of iNOS and COX-2 and induced HO-1 expression. It also prevented nuclear translocation of NF-κB by inhibiting the phosphorylation and degradation of IκBα. Furthermore, the phosphorylation of MAPKs in LPS-stimulated RAW 264.7 cells was significantly inhibited by RRE. These findings suggest that RRE may operate as an effective anti-inflammatory agent by inhibiting the activation of NF-κB and MAPK signaling pathways and inducing HO-1 expression in macrophages. Our results suggest that RRE has potential value as candidate to inflammatory therapeutic phytomedicine.
机译:Rhapontici Radix(RR)已在东亚用于传统医学中,并已显示出多种有益作用。然而,其关于炎症相关疾病的生物学特性或机理尚不清楚。这项研究的目的是确定根茎乙醇提取物(RRE)的抗炎活性和潜在的分子机制。 RRE对LPS刺激的巨噬细胞中NO,细胞因子,炎性相关蛋白和mRNA产生的抑制作用分别通过Griess分析,ELISA,Western印迹分析和实时RT-PCR确定。我们的结果表明,RRE处理可显着抑制RAW 264.7细胞和小鼠腹膜巨噬细胞中NO的分泌和炎性细胞因子,而无细胞毒性。我们还发现RRE强烈抑制iNOS和COX-2的表达并诱导HO-1的表达。它还通过抑制IκBα的磷酸化和降解来防止NF-κB的核易位。此外,RRE显着抑制了LPS刺激的RAW 264.7细胞中MAPK的磷酸化。这些发现表明,RRE可以通过抑制NF-κB和MAPK信号通路的激活并诱导巨噬细胞中HO-1的表达来作为有效的抗炎药。我们的结果表明,RRE具有潜在的潜在价值,可作为炎症性治疗植物药的候选药物。

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