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Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

机译:通过NF-κB信号通路灭活司马糖醇对脂多糖刺激RAW264.7细胞的抗炎作用

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摘要

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of . In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.
机译:Simonsinol是一个自然的Sesqui-Neolignan首先从树皮中孤立。在这项研究中,用脂多糖(LPS) - 刺激的鼠巨噬细胞Raw264.7细胞模型研究了Simonsinol的抗炎活性。结果表明,西蒙诺酚可以拮抗LPS对Raw264.7细胞的形态变化的影响,并降低一氧化氮(NO),肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)的产生。通过GRIESS测定和酶联免疫吸附测定(ELISA)确定的LPS刺激的RAW264.7细胞。此外,Simonsinol可以通过逆转录聚合酶链反应(RT-PCR)测量,并抑制NF-κB的α抑制剂的磷酸化(IκBα的α抑制剂(IκBα)的磷酸化(IκBα)的磷酸化(IκBα )被蛋白质印迹测定。总之,这些数据表明,席梦思素可以通过核转录因子Kappa-B(NF-κB)信号通路的灭活来抑制LPS刺激的Raw264.7细胞中的炎症反应。

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