Apigenin Inhibits Tumor Necrosis Factor-alpha-Induced Production and Gene Expression of Mucin through Regulating Nuclear Factor-Kappa B Signaling Pathway in Airway Epithelial Cells
Biomolecules & Therapeutics
; : 525-531, 2014.
Article
em En
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| ID: wpr-185391
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WPRO
ABSTRACT
In the present study, we investigated whether apigenin significantly affects tumor necrosis factor-alpha (TNF-alpha)-induced production and gene expression of MUC5AC mucin in airway epithelial cells. Confluent NCI-H292 cells were pretreated with apigenin for 30 min and then stimulated with TNF-alpha for 24 h or the indicated periods. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Apigenin significantly inhibited MUC5AC mucin production and down-regulated MUC5AC gene expression induced by TNF-alpha in NCI-H292 cells. To elucidate the action mechanism of apigenin, effect of apigenin on TNF-alpha-induced nuclear factor kappa B (NF-kappaB) signaling pathway was also investigated by western blot analysis. Apigenin inhibited NF-kappaB activation induced by TNF-alpha. Inhibition of inhibitory kappa B kinase (IKK) by apigenin led to the suppression of inhibitory kappa B alpha (IkappaBalpha) phosphorylation and degradation, p65 nuclear translocation. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. Apigenin also has an influence on upstream signaling of IKK because it inhibited the expression of adaptor protein, receptor interacting protein 1 (RIP1). These results suggest that apigenin can regulate the production and gene expression of mucin through regulating NF-kappaB signaling pathway in airway epithelial cells.
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Assunto principal:
Fosforilação
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Fosfotransferases
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Ensaio de Imunoadsorção Enzimática
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Regulação para Baixo
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Expressão Gênica
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Western Blotting
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Reação em Cadeia da Polimerase
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NF-kappa B
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Fator de Necrose Tumoral alfa
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Apigenina
Idioma:
En
Revista:
Biomolecules & Therapeutics
Ano de publicação:
2014
Tipo de documento:
Article