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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.
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页码:431 / 436
页数:6
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