Diclofenac Inhibits Phorbol Ester-Induced Gene Expression and Production of MUC5AC Mucin via Affecting Degradation of IkBα and Translocation of NF-kB p65 in NCl-H292 Cells

被引:8
|
作者
Jin, Fengri [1 ]
Li, Xin [1 ]
Lee, Hyun Jae [2 ,3 ]
Lee, Choong Jae [1 ]
机构
[1] Chungnam Natl Univ, Sch Med, Dept Pharmacol, Daejeon 35015, South Korea
[2] Sahmyook Univ, Smith Liberal Arts Coll, Seoul 01795, South Korea
[3] Sahmyook Univ, Dept Addict Sci, Grad Sch, Seoul 01795, South Korea
基金
新加坡国家研究基金会;
关键词
MUC5AC; Pulmonary mucin; Diclofenac; KAPPA-B ACTIVATION; EPIDERMAL-GROWTH-FACTOR; AIRWAY EPITHELIAL-CELLS; SIGNALING PATHWAY; MUCUS; APIGENIN; WOGONIN; AGENTS; ROOT;
D O I
10.4062/biomolther.2020.090
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, diclofenac, a non-steroidal anti-inflammatory drug, was investigated for its potential effect on the gene expression and production of airway MUC5AC mucin. The human respiratory epithelial NCI-H292 cells were pretreated with diclofenac for 30 min and stimulated with phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect of diclofenac on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated. Diclofenac suppressed the production and gene expression of MUC5AC mucins, induced by PMA through the inhibition of degradation of inhibitory kappa B alpha (1kB alpha) and NF-kB p65 nuclear translocation. These results suggest diclofenac regulates the gene expression and production of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.
引用
收藏
页码:431 / 436
页数:6
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