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首页> 外文期刊>Biomolecules & therapeutics >Apigenin Inhibits Tumor Necrosis Factor-alpha-Induced Production and Gene Expression of Mucin through Regulating Nuclear Factor-Kappa B Signaling Pathway in Airway Epithelial Cells
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Apigenin Inhibits Tumor Necrosis Factor-alpha-Induced Production and Gene Expression of Mucin through Regulating Nuclear Factor-Kappa B Signaling Pathway in Airway Epithelial Cells

机译：芹菜素通过调节气道上皮细胞中的核因子-κB信号通路抑制肿瘤坏死因子-α诱导的黏蛋白的生产和基因表达。

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In the present study, we investigated whether apigenin significantly affects tumor necrosis factor-alpha (TNF-alpha)-induced production and gene expression of MUC5AC mucin in airway epithelial cells. Confluent NCI-H292 cells were pretreated with apigenin for 30 min and then stimulated with TNF-alpha for 24 h or the indicated periods. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Apigenin significantly inhibited MUC5AC mucin production and down-regulated MUC5AC gene expression induced by TNF-alpha in NCI-H292 cells. To elucidate the action mechanism of apigenin, effect of apigenin on TNF-alpha-induced nuclear factor kappa B (NF-kappa B) signaling pathway was also investigated by western blot analysis. Apigenin inhibited NF-kappa B activation induced by TNF-alpha. Inhibition of inhibitory kappa B kinase (IKK) by apigenin led to the suppression of inhibitory kappa B alpha (I kappa B alpha) phosphorylation and degradation, p65 nuclear translocation. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. Apigenin also has an influence on upstream signaling of IKK because it inhibited the expression of adaptor protein, receptor interacting protein 1 (RIP1). These results suggest that apigenin can regulate the production and gene expression of mucin through regulating NF-kappa B signaling pathway in airway epithelial cells.
机译：在本研究中，我们调查芹菜素是否显着影响肿瘤坏死因子-α（TNF-alpha）诱导的气道上皮细胞中MUC5AC粘蛋白的产生和基因表达。将融合的NCI-H292细胞用芹菜素预处理30分钟，然后用TNF-α刺激24小时或指定的时间。分别通过逆转录-聚合酶链反应（RT-PCR）和酶联免疫吸附测定（ELISA）测量MUC5AC粘蛋白的基因表达和粘蛋白蛋白的产生。芹菜素显着抑制NCI-H292细胞中TNF-α诱导的MUC5AC粘蛋白生成并下调MUC5AC基因表达。为了阐明芹菜素的作用机理，还通过蛋白质印迹分析研究了芹菜素对TNF-α诱导的核因子κB（NF-κB）信号传导途径的作用。芹菜素抑制由TNF-α诱导的NF-κB活化。芹菜素对抑制性κB激酶（IKK）的抑制导致抑制性抑制性κB（IκBα）的磷酸化和降解，p65核易位。反过来，这导致NCI-H292细胞中MUC5AC蛋白产生的下调。芹菜素也对IKK的上游信号传导有影响，因为它抑制了衔接蛋白，受体相互作用蛋白1（RIP1）的表达。这些结果表明芹菜素可以通过调节气道上皮细胞中的NF-κB信号传导通路来调节粘蛋白的产生和基因表达。

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