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首页> 外文期刊>Life sciences >Luteolin suppresses inflammation-associated gene expression by blocking NF-kappa B and AP-1 activation pathway in mouse alveolar macrophages
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Luteolin suppresses inflammation-associated gene expression by blocking NF-kappa B and AP-1 activation pathway in mouse alveolar macrophages

机译：木犀草素通过阻断小鼠肺泡巨噬细胞中的NF-κB和AP-1激活途径来抑制炎症相关基因的表达

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Luteolin. a plant flavonoid, has potent anti-inflammatory proper-ties both in vitro and in vivo. However, the molecular mechanism of luteolin-mediated immune modulation has not been fully understood. In this study, we examined the effects of luteolin on the production of nitric oxide (NO) and prostaglandin E-2 (PGE(2)), as well as the expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) in mouse alveolar macrophage MH-S and peripheral macrophage RAW 264.7 cells. Luteolin dose-dependently inhibited the expression and production of these inflammatory genes and mediators in macrophages stimulated with lipopolysaccharide (LPS). Semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR) assay further confirmed the suppression of LPS-induced TNF- alpha, IL-6, iNOS and COX-2 gene expression by luteolin at a transcriptional level. Luteolin also reduced the DNA binding activity of nuclear factor-kappa B (NF-kappa B) in LPS-activated macrophages. Moreover, luteolin blocked the degradation of I kappa B-alpha and nuclear translocation of NF-kappa B p65 subunit. In addition, luteolin significantly inhibited the LPS-induced DNA binding activity of activating protein-1 (AP-1). We also found that luteolin attenuated the LPS-mediated protein kinase B (Akt) and IKK phosphorylation, as well as reactive oxygen species (ROS) production. In sum, these data suggest that, by blocking NF-kappa B and AP-1 activation, luteolin acts to suppress the LPS-elicited inflammatory events in mouse alveolar macrophages, and this effect was mediated, at least in part, by inhibiting the generation of reactive oxygen species. Our observations suggest a possible therapeutic application of this agent for treating inflammatory disorders in lung. (C) 2007 Elsevier Inc. All rights reserved.
机译：木犀草素。一种植物类黄酮，在体外和体内均具有有效的抗炎特性。然而，木犀草素介导的免疫调节的分子机制尚未完全了解。在这项研究中，我们研究了木犀草素对一氧化氮（NO）和前列腺素E-2（PGE（2））的产生以及诱导型一氧化氮合酶（iNOS），环氧合酶2（COX- 2），小鼠肺泡巨噬细胞MH-S和外周巨噬细胞RAW 264.7细胞中的肿瘤坏死因子-α（TNF-α）和白介素6（IL-6）。木犀草素剂量依赖性地抑制脂多糖（LPS）刺激的巨噬细胞中这些炎症基因和介质的表达和产生。半定量逆转录聚合酶链反应（RT-PCR）分析进一步证实了木犀草素在转录水平上抑制LPS诱导的TNF-α，IL-6，iNOS和COX-2基因表达。木犀草素还降低了LPS激活的巨噬细胞中核因子-κB（NF-κB）的DNA结合活性。此外，木犀草素阻断了IκB-α的降解和NF-κBp65亚基的核易位。此外，木犀草素显着抑制LPS诱导的活化蛋白1（AP-1）的DNA结合活性。我们还发现木犀草素减弱了LPS介导的蛋白激酶B（Akt）和IKK磷酸化以及活性氧（ROS）的产生。总之，这些数据表明，木犀草素通过阻断NF-κB和AP-1的活化，抑制小鼠肺泡巨噬细胞中LPS引起的炎症事件，并且至少部分地通过抑制这种生成来介导这种作用。活性氧种类我们的观察结果表明该药物可能用于治疗肺部炎症。 （C）2007 Elsevier Inc.保留所有权利。

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