Regulation of Tumor Necrosis Factor-alpha-induced Airway Mucin Production and Gene Expression by Carbenoxolone, Prunetin, and Silibinin.
10.4046/trd.2010.69.5.348
- Author:
Hyun Jae LEE
1
;
Su Yel LEE
;
Byeong Kyou JEON
;
Jae Woo LEE
;
Mi Nam LEE
;
Ju Ock KIM
;
Choong Jae LEE
Author Information
1. Department of Pharmacology, Chungnam National University School of Medicine, Daejeon, Korea. LCJ123@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
MUC5AC protein, human;
Carbenoxolone;
Prunetin;
Silibinin
- MeSH:
Carbenoxolone;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells;
Gene Expression;
Humans;
Isoflavones;
Mucin 5AC;
Mucins;
Necrosis;
Silymarin;
Tumor Necrosis Factor-alpha
- From:Tuberculosis and Respiratory Diseases
2010;69(5):348-353
- CountryRepublic of Korea
- Language:English
-
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.
