Regulation of Tumor Necrosis Factor-alpha-induced Airway Mucin Production and Gene Expression by Carbenoxolone, Prunetin, and Silibinin / 결핵및호흡기질환
Tuberculosis and Respiratory Diseases
; : 348-353, 2010.
Article
en En
| WPRIM
| ID: wpr-204137
Biblioteca responsable:
WPRO
ABSTRACT
BACKGROUND: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-alpha-induced MUC5AC mucin production and gene expression from human airway epithelial cells. METHODS: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-alpha for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. RESULTS: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-alpha; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-alpha. CONCLUSION: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-alpha, by directly acting on airway epithelial cells.
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Índice:
WPRIM
Asunto principal:
Silimarina
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Ensayo de Inmunoadsorción Enzimática
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Carbenoxolona
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Expresión Génica
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Factor de Necrosis Tumoral alfa
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Células Epiteliales
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Mucina 5AC
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Isoflavonas
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Mucinas
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Necrosis
Límite:
Humans
Idioma:
En
Revista:
Tuberculosis and Respiratory Diseases
Año:
2010
Tipo del documento:
Article