Lee Hyun Jae, Seo Hyo-Seok, Ryu Jiho, Yoon Yong Pill, Park Su Hyun, Lee Choong Jae
Department of Pharmacology, School of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Department of Pharmacology, School of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Pulm Pharmacol Ther. 2015 Apr;31:117-22. doi: 10.1016/j.pupt.2014.09.008. Epub 2014 Oct 5.
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-κB 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 Bα (IκBα); (4) Luteolin inhibited PMA-induced phosphorylation and nuclear translocation of nuclear factor kappa B (NF-κB) 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.
木犀草素是一种从忍冬和野菊花中提取的黄酮类化合物,据报道具有抗炎、抗氧化和抗癌作用。在本研究中,我们调查了木犀草素是否会显著影响气道粘蛋白的分泌、产生和基因表达。将汇合的NCI-H292细胞用木犀草素预处理30分钟,然后用表皮生长因子(EGF)或佛波酯(PMA)刺激24小时或指定时间。通过RT-PCR检测MUC5AC粘蛋白基因的表达。通过ELISA检测MUC5AC粘蛋白的产生和分泌。为了阐明木犀草素的作用机制,通过蛋白质免疫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粘蛋白分泌;(2)木犀草素抑制EGF或PMA诱导的MUC5AC粘蛋白产生及MUC5AC粘蛋白基因表达;(3)木犀草素抑制PMA诱导的抑制性κBα(IκBα)磷酸化和降解;(4)木犀草素抑制PMA诱导的核因子κB(NF-κB)p65磷酸化和核转位。该结果表明,木犀草素可通过调节NF-κB信号通路作用于气道上皮细胞,从而调节粘蛋白的分泌、产生和基因表达。