Apigenin and Wogonin Regulate Epidermal Growth Factor Receptor Signaling Pathway Involved in MUC5AC Mucin Gene Expression and Production from Cultured Airway Epithelial Cells.
10.4046/trd.2014.76.3.120
- Author:
Md Asaduzzaman SIKDER
1
;
Hyun Jae LEE
;
Jiho RYU
;
Su Hyun PARK
;
Ju Ock KIM
;
Jang Hee HONG
;
Jeong Ho SEOK
;
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:
Receptor, Epidermal Growth Factor;
Mucins;
Wogonin;
Apigenin
- MeSH:
Apigenin*;
Epidermal Growth Factor*;
Epithelial Cells*;
Gene Expression*;
Humans;
Mucins*;
Phosphorylation;
Receptor, Epidermal Growth Factor*
- From:Tuberculosis and Respiratory Diseases
2014;76(3):120-126
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: We investigated whether wogonin and apigenin significantly affect the epidermal growth factor receptor (EGFR) signaling pathway involved in MUC5AC mucin gene expression, and production from cultured airway epithelial cells; this was based on our previous report that apigenin and wogonin suppressed MUC5AC mucin gene expression and production from human airway epithelial cells. METHODS: Confluent NCI-H292 cells were pretreated with wogonin or apigenin for 15 minutes or 24 hours and then stimulated with epidermal growth factor (EGF) for 24 hours or the indicated periods. RESULTS: We found that incubation of NCI-H292 cells with wogonin or apigenin inhibited the phosphorylation of EGFR. The downstream signals of EGFR such as phosphorylation of MEK1/2 and ERK1/2 were also inhibited by wogonin or apigenin. CONCLUSION: The results suggest that wogonin and apigenin inhibits EGFR signaling pathway, which may explain how they inhibit MUC5AC mucin gene expression and production induced by EGF.