Effect of Prunetin on TNF-alpha-Induced MUC5AC Mucin Gene Expression, Production, Degradation of IkappaB and Translocation of NF-kappaB p65 in Human Airway Epithelial Cells.
10.4046/trd.2013.75.5.205
- Author:
Jiho RYU
1
;
Hyun Jae LEE
;
Su Hyun PARK
;
Md Asaduzzaman SIKDER
;
Ju Ock KIM
;
Jang Hee HONG
;
Jeong Ho SEOK
;
Choong Jae LEE
Author Information
1. Department of Pharmacology, Chungnam National University Hospital, Chungnam National University School of Medicine, Daejeon, Korea. LCJ123@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
Mucins;
MUC5AC Protein, Human;
Prunetin
- MeSH:
Blotting, Western;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells*;
Gene Expression*;
Humans*;
Isoflavones;
Mucin 5AC;
Mucins*;
NF-kappa B*;
Polymerase Chain Reaction;
Reverse Transcription;
Tumor Necrosis Factor-alpha
- From:Tuberculosis and Respiratory Diseases
2013;75(5):205-209
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: We investigated whether prunetin significantly affects tumor necrosis factor-alpha (TNF-alpha)-induced MUC5AC mucin gene expression, production, inhibitory kappa B (IkappaB) degradation and nuclear factor kappa B (NF-kappaB) p65 translocation in human airway epithelial cells. METHODS: Confluent NCI-H292 cells were pretreated with prunetin for 30 minutes and then stimulated with TNF-alpha for 24 hours or the indicated periods. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The effect of prunetin on TNF-alpha-induced degradation of IkappaB and translocation of NF-kappaB p65 was investigated by western blot analysis. RESULTS: We found that incubation of NCI-H292 cells with prunetin significantly inhibited mucin production and down-regulated the MUC5AC gene expression induced by TNF-alpha. Prunetin inhibited TNF-alpha-induced degradation of IkappaB and translocation of NF-kappaB p65. CONCLUSION: This result suggests that prunetin inhibits the NF-kappaB signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production regulated by the NF-kappaB signaling pathway.
