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Tuberculosis & Respiratory Diseases

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Vol.69 No.5
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Regulation of Tumor Necrosis Factor-α-induced Airway Mucin Production and Gene Expression by Carbenoxolone, Prunetin, and Silibinin

Tuberculosis & Respiratory Diseases / Tuberculosis & Respiratory Diseases,
2010, v.69 no.5, pp.348-353
Hyun Jae Lee (Chungnam National University)
Su Yel Lee (Chungnam National University)
Byeong Kyou Jeon (Daegu Health College)
Jae Woo Lee (LG Life Science)
Mi Nam Lee (Chungnam National University)


Hyun, J. L. , Su, Y. L. , Byeong, K. J. , Jae, W. L. , Mi, N. L. , & (2010). Regulation of Tumor Necrosis Factor-α-induced Airway Mucin Production and Gene Expression by Carbenoxolone, Prunetin, and Silibinin. Tuberculosis & Respiratory Diseases, 69(5), 348-353.
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Abstract

Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-α- 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-α 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-α; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-α. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-α, by directly acting on airway epithelial cells.

keywords
MUC5AC protein, human, Carbenoxolone, Prunetin, Silibinin

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