Pyronaridine Inhibited MUC5AC Mucin Gene Expression by Regulation of Nuclear Factor Kappa B Signaling Pathway in Human Pulmonary Mucoepidermoid Cells

被引:0
作者
Hossain, Rajib [1 ,2 ]
Lee, Hyun Jae [3 ]
Lee, Choong Jae [1 ,2 ]
机构
[1] Chungnam Natl Univ, Sch Med, Dept Pharmacol, Daejeon 35015, South Korea
[2] Chungnam Natl Univ, Brain Korea FOUR Project Med Sci 21, Daejeon 35015, South Korea
[3] Sahmyook Univ, Smith Liberal Arts Coll, Seoul 01795, South Korea
关键词
MUC5AC; Pulmonary mucin; Pyronaridine; AIRWAY EPITHELIAL-CELLS; MUC5AC MUCIN; PHORBOL ESTER; ACTIVATION; INHIBITION; APIGENIN; ROOT; P65;
D O I
10.4062/biomolther.2024.072
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In this study, the potential effects of pyronaridine, an antimalarial agent, on airway MUC5AC mucin gene expression were investigated. The human pulmonary epithelial NCI-H292 cells were pretreated with pyronaridine for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h. The effect of pyronaridine on the PMA-induced nuclear factor kappa B (NF-kappa B) kappa B) signaling pathway was also examined. Pyronaridine inhibited glycoprotein production and mRNA expression of MUC5AC mucins induced by PMA through the inhibition of degradation of inhibitory kappa B alpha alpha and NF-kappa B kappa B p65 nuclear translocation. These results suggest that pyronaridine suppresses gene expression of mucin through regulation of the NF-kappa B kappa B signaling pathway in human pulmonary epithelial cells.
引用
收藏
页码:540 / 545
页数:6
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