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자료유형
학술저널
저자정보
Sikder, Md. Asaduzzaman (Department of Pharmacology, Chungnam National University School of Medicine) Lee, Hyun Jae (Department of Pharmacology, Chungnam National University School of Medicine) Ryu, Jiho (Department of Pharmacology, Chungnam National University School of Medicine) Park, Su Hyun (Department of Pharmacology, Chungnam National University School of Medicine) Kim, Ju-Ock (Pulmonology Section, Department of Internal Medicine, Chungnam National University Hospital, Chungnam National University School of Medicine) Hong, Jang-Hee (Department of Pharmacology, Chungnam National University School of Medicine) Seok, Jeong Ho (Department of Pharmacology, Chungnam National University School of Medicine) Lee, Choong Jae (Department of Pharmacology, Chungnam National University School of Medicine)
저널정보
대한결핵 및 호흡기학회 Tuberculosis and Respiratory Diseases 결핵 및 호흡기 질환 제76권 제3호
발행연도
2014.1
수록면
120 - 126 (7page)

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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.

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