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首頁> 美國衛(wèi)生研究院文獻>Biomolecules Therapeutics >Emodin Inhibited MUC5AC Mucin Gene Expression via Affecting EGFR-MAPK-Sp1 Signaling Pathway in Human Airway Epithelial Cells
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Emodin Inhibited MUC5AC Mucin Gene Expression via Affecting EGFR-MAPK-Sp1 Signaling Pathway in Human Airway Epithelial Cells

機譯:大黃素通過影響人氣道上皮細胞中的 EGFR-MAPK-SP1 信號通路抑制 MUC5AC 粘蛋白基因表達

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摘要

The aim of this study was to evaluate emodin, a natural trihydroxyanthraquinone compound found in the roots and barks of several plants including rhubarb and buckthorn, might attenuate epidermal growth factor (EGF)-induced airway MUC5AC mucin gene expression. The human pulmonary mucoepidermoid NCI-H292 cells were pretreated with for 30 min and then stimulated with EGF for the following 24 h. The effect of emodin on EGF-induced mitogen-activated protein kinase (MAPK) signaling pathway was examined. As a result, emodin blocked the expression of MUC5AC mucin mRNA and production of mucous glycoprotein via suppressing the phosphorylation of EGF receptor (EGFR), phosphorylation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) 1 and 2 (MEK1/2), phosphorylation of p38 MAPK, phosphorylation of ERK 1/2 (p44/42), and the nuclear expression of specificity protein-1 (Sp1). These findings imply that emodin has a potential to mitigate EGF-stimulated mucin gene expression by inhibiting the EGFR-MAPK-Sp1 signaling pathway, in NCI-H292 cells.
機譯:本研究的目的是評估大黃素,一種天然的三羥基蒽醌化合物,存在于包括大黃和沙棘在內的幾種植物的根和樹皮中,可能會減弱表皮生長因子 (EGF) 誘導的氣道 MUC5AC 粘蛋白基因表達。人肺粘液表皮樣 NCI-H292 細胞預處理 30 min,然后用 EGF 刺激 24 h。檢查大黃素對 EGF 誘導的絲裂原活化蛋白激酶 (MAPK) 信號通路的影響。結果,大黃素通過抑制 EGF 受體 (EGFR) 的磷酸化、絲裂原活化蛋白激酶 (MAPK)/細胞外信號調節(jié)激酶 (ERK) 1 和 2 (MEK1/2)、p38 MAPK 的磷酸化、ERK 1/2 的磷酸化 (p44/42) 和特異性蛋白-1 (Sp1) 的核表達來阻斷 MUC5AC 粘蛋白 mRNA 的表達和粘液糖蛋白的產(chǎn)生。這些發(fā)現(xiàn)表明,大黃素有可能通過抑制 NCI-H292 細胞中的 EGFR-MAPK-Sp1 信號通路來減輕 EGF 刺激的粘蛋白基因表達。

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