首页> 外文期刊>Pulmonary pharmacology & therapeutics >Luteolin inhibited the gene expression, production and secretion of MUC5AC mucin via regulation of nuclear factor kappa B signaling pathway in human airway epithelial cells
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Luteolin inhibited the gene expression, production and secretion of MUC5AC mucin via regulation of nuclear factor kappa B signaling pathway in human airway epithelial cells

机译:木犀草素通过调节人气道上皮细胞中核因子κB信号通路抑制MUC5AC粘蛋白的基因表达,产生和分泌

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Luteolin, a flavonoidal compound derived from Lonicera japonica Thunb. and Chrysanthemum indicum L, has been reported to show anti-inflammatory, anti-oxidative and anti-carcinogenic effects. In this study, we investigated whether luteolin significantly affects the secretion, production and gene expression of airway mucin. Confluent NCI-H292 cells were pretreated with luteolin for 30 min and then stimulated with EGF (epidermal growth factor) or PMA (phorbol 12-myristate 13-acetate) for 24 h or the indicated periods. The MUC5AC mucin gene expression was measured by RT-PCR. Production and secretion of MUC5AC mucin protein were measured by ELISA. To elucidate the action mechanism of luteolin, effect of luteolin on PMA-induced NF-kappaB signaling pathway was investigated by western blot analysis. The results were as follows: (1) Luteolin inhibited the secretion of MUC5AC mucin protein induced by EGF or PMA; (2) Luteolin inhibited the production of MUC5AC mucin protein and the expression of MUC5AC mucin gene induced by EGF or PMA; (3) Luteolin inhibited PMA-induced phosphorylation and degradation of inhibitory kappa Balpha (IkBoc); (4) Luteolin inhibited PMA-induced phosphorylation and nuclear trans-location of nuclear factor kappa B (NF-kB) p65. This result suggests that luteolin can regulate the secretion, production and gene expression of mucin by acting on airway epithelial cells via regulation of NF-kB signaling pathway.
机译:木犀草素,一种源自忍冬忍冬的类黄酮化合物。据报道,菊花和印度菊花具有抗炎,抗氧化和抗癌的作用。在这项研究中,我们调查了木犀草素是否显着影响气道黏蛋白的分泌,产生和基因表达。融合的NCI-H292细胞用木犀草素预处理30分钟,然后用EGF(表皮生长因子)或PMA(佛波12-肉豆蔻酸酯13-乙酸酯)刺激24小时或指定的时间。通过RT-PCR测量MUC5AC粘蛋白基因表达。通过ELISA测量MUC5AC粘蛋白的产生和分泌。为了阐明木犀草素的作用机理,通过蛋白质印迹分析研究了木犀草素对PMA诱导的NF-κB信号通路的影响。结果如下:(1)木犀草素抑制EGF或PMA诱导的MUC5AC粘蛋白的分泌; (2)木犀草素抑制EGF或PMA诱导的MUC5AC粘蛋白蛋白的产生和MUC5AC粘蛋白基因的表达; (3)木犀草素抑制PMA诱导的磷酸化和抑制性κBα(IkBoc)的降解; (4)木犀草素抑制PMA诱导的磷酸化和核因子κB(NF-kB)p65的核转位。该结果表明,木犀草素可以通过调节NF-kB信号通路,通过作用于气道上皮细胞来调节粘蛋白的分泌,产生和基因表达。

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