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首页> 外文期刊>Cytokine >Quercetin 3-O-beta-(2''-galloyl)-glucopyranoside inhibits endotoxin LPS-induced IL-6 expression and NF-kappaB activation in macrophages.
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Quercetin 3-O-beta-(2''-galloyl)-glucopyranoside inhibits endotoxin LPS-induced IL-6 expression and NF-kappaB activation in macrophages.

机译：槲皮素3-O-β-（2''-galloyl）-吡喃葡萄糖苷抑制内毒素LPS诱导巨噬细胞中IL-6表达和NF-κB活化。

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摘要

We previously isolated quercetin 3-O-beta-(2''-galloyl)-glucopyranoside (QG-32) from Persicaria lapathifolia (Polygonacease) as an inhibitor of superoxide production. In the present study, QG-32 was found to inhibit interleukin (IL)-6 production in endotoxin lipopolysaccharide (LPS)-stimulated macrophages RAW 264.7. The QG-32 attenuated LPS-induced synthesis of IL-6 transcript but also inhibited IL-6 promoter activity, indicating that the compound could down-regulate LPS-induced IL-6 expression at the transcription level. Since nuclear factor (NF)-kappaB has been evidenced to play a major mechanism in the LPS-induced IL-6 expression, an effect of QG-32 on NF-kappaB activating pathway was further analyzed. QG-32 inhibited nuclear import as well as DNA binding activity of NF-kappaB complex and subsequently suppressed NF-kappaB transcriptional activity in LPS-stimulated macrophages. However, QG-32 affected neither LPS-induced inhibitory kappaB (IkappaB) degradation nor IkappaB kinase (IKK) activation. In another experiment, QG-32 inhibited expression vector encoding NF-kappaB p65 or p50-elicited IL-6 promoter activity. Taken together, QG-32 could inhibit NF-kappaB-dependent IL-6 expression, targeting nuclear translocation of NF-kappaB complex downstream IkappaB degradation. This mechanism of action would be different from that of quercetin, an aglycone of QG-32, targeting IKK upstream IkappaB degradation. Finally, this study could provide a pharmacological potential of QG-32 in the inflammatory disorders.
机译：我们先前从桃蚜（Posicaria lapathifolia（Polygonacease））中分离了槲皮素3-O-β-（2''-galloyl）-吡喃葡萄糖苷（QG-32）作为超氧化物生产的抑制剂。在本研究中，发现QG-32抑制内毒素脂多糖（LPS）刺激的巨噬细胞RAW 264.7中白介素（IL）-6的产生。 QG-32减弱了LPS诱导的IL-6转录物的合成，但也抑制了IL-6启动子的活性，表明该化合物可以在转录水平下调LPS诱导的IL-6的表达。由于已经证明核因子（NF）-κB在LPS诱导的IL-6表达中起主要作用，因此将进一步分析QG-32对NF-κB激活途径的影响。 QG-32抑制核输入以及NF-κB复合物的DNA结合活性，并随后抑制LPS刺激的巨噬细胞中的NF-κB转录活性。但是，QG-32既不影响LPS诱导的抑制性kappaB（IkappaB）降解，也不影响IkappaB激酶（IKK）激活。在另一个实验中，QG-32抑制了编码NF-kappaB p65或p50引起的IL-6启动子活性的表达载体。综上所述，QG-32可以抑制NF-κB依赖的IL-6表达，靶向NF-κB复合物下游IkappB降解的核易位。这种作用机制与QK-32苷元槲皮素的作用机制不同，它是针对IKK上游IkappaB降解的。最后，这项研究可以提供QG-32在炎症性疾病中的药理潜力。

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