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Sikder, Md. Asaduzzaman,Lee, Hyun Jae,Ryu, Jiho,Park, Su Hyun,Kim, Ju-Ock,Hong, Jang-Hee,Seok, Jeong Ho,Lee, Choong Jae The Korean Academy of Tuberculosis and Respiratory 2014 Tuberculosis and Respiratory Diseases Vol.76 No.3
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.
( Md. Asaduzzaman Sikder ),( Hyun Jae Lee ),( Ji Ho Ryu ),( Su Hyun Park ),( Ju Ock Kim ),( Jang Hee Hong ),( Jeong Ho Seok ),( Choong Jae Lee ) 대한결핵 및 호흡기학회 2014 Tuberculosis and Respiratory Diseases Vol.76 No.3
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.
( Md. Asaduzzaman Sikder ),( Hyun Jae Lee ),( Su Yel Lee ),( Heung Seog Bae ),( Jang Hyun Kim ),( Gyu Tae Chang ),( Choong Jae Lee ) 한국응용약물학회 2011 Biomolecules & Therapeutics(구 응용약물학회지) Vol.19 No.3
We conducted this study to investigate whether berberine significantly affects MUC5AC mucin gene expression and mucin production induced by epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-α (TNF-α) from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of berberine for 30 min and then stimulated with EGF, PMA or TNF-α for 24 h. MUC5AC mucin gene expression and mucin production were measured by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Berberine was found to inhibit the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-α. Berberine also inhibited the production of MUC5AC mucin protein stimulated by the same inducers. This result suggests that berberine can regulate the expression of mucin gene and production of mucin protein, by directly acting on human airway epithelial cells.
( Hyo Seok Seo ),( Mohamed Asaduzzaman Sikder ),( Hyun Jae Lee ),( Jiho Ryu ),( Choong Jae Lee ) 한국응용약물학회 2014 Biomolecules & Therapeutics(구 응용약물학회지) Vol.22 No.6
In the present study, we investigated whether apigenin significantly affects tumor necrosis factor-α (TNF-α)-induced production and gene expression of MUC5AC mucin in airway epithelial cells. Confluent NCI-H292 cells were pretreated with apigenin for 30 min and then stimulated with TNF-α for 24 h or the indicated periods. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Apigenin significantly inhibited MUC5AC mucin production and down-regulated MUC5AC gene expression induced by TNF-α in NCI-H292 cells. To elucidate the action mechanism of apigenin, effect of apigenin on TNF-α-induced nuclear factor kappa B (NF-κB) signaling pathway was also investigated by western blot analysis. Apigenin inhibited NF-κB activation induced by TNF-α. Inhibition of inhibitory kappa B kinase (IKK) by apigenin led to the suppression of inhibitory kappa B alpha (IκBα) phosphorylation and degradation, p65 nuclear translocation. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. Apigenin also has an influence on upstream signaling of IKK because it inhibited the expression of adaptor protein, receptor interacting protein 1 (RIP1). These results suggest that apigenin can regulate the production and gene expression of mucin through regulating NF-κB signaling pathway in airway epithelial cells.
Shin, Hyun-Dae,Lee, Hyun Jae,Sikder, Asaduzzaman Md.,Park, Su Hyun,Ryu, Jiho,Hong, Jang-Hee,Kim, Ju-Ock,Seok, Jeong Ho,Lee, Choong Jae The Korean Academy of Tuberculosis and Respiratory 2012 Tuberculosis and Respiratory Diseases Vol.73 No.4
Background: We investigated whether chrysin affected MUC5AC mucin production and gene expression induced by phorbol ester (phorbol 12-myristate 13-acetate, PMA) or epidermal growth factor (EGF) from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with varying concentrations of chrysin for 30 minutes, and were then stimulated with PMA and EGF for 24 hours, respectively. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Results: Concentrations of $10{\mu}M$ and $100{\mu}M$ chrysin were found to inhibit the production of MUC5AC mucin protein induced by PMA; A concentration of $100{\mu}M$ chrysin also inhibited the production of MUC5AC mucin protein induced by EGF; $100{\mu}M$ chrysin inhibited the expression of MUC5AC mucin gene induced by PMA or EGF. The cytotoxicity of chrysin was checked by lactate dehydrogenase assay, and there was no cytotoxic effect observed for chrysin. Conclusion: These results suggest that chrysin can inhibit mucin gene expression and the production of mucin protein by directly acting on airway epithelial cells.
( Hyun Dae Shin ),( Hyun Jae Lee ),( Asaduzzaman Sikder ),( Su Hyun Park ),( Jiho Ryu ),( Jang Hee Hong ),( Ju Ock Kim ),( Jeong Ho Seok ),( Choong Jae Lee ) 대한결핵 및 호흡기학회 2012 Tuberculosis and Respiratory Diseases Vol.73 No.4
Background: We investigated whether chrysin affected MUC5AC mucin production and gene expression induced by phorbol ester (phorbol 12-myristate 13-acetate, PMA) or epidermal growth factor (EGF) from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with varying concentrations of chrysin for 30 minutes, and were then stimulated with PMA and EGF for 24 hours, respectively. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Results: Concentrations of 10μM and 100μM chrysin were found to inhibit the production of MUC5AC mucin protein induced by PMA; A concentration of 100μM chrysin also inhibited the production of MUC5AC mucin protein induced by EGF; 100μM chrysin inhibited the expression of MUC5AC mucin gene induced by PMA or EGF. The cytotoxicity of chrysin was checked by lactate dehydrogenase assay, and there was no cytotoxic effect observed for chrysin. Conclusion: These results suggest that chrysin can inhibit mucin gene expression and the production of mucin protein by directly acting on airway epithelial cells.
Ryu, Jiho,Lee, Hyun Jae,Park, Su Hyun,Sikder, Md. Asaduzzaman,Kim, Ju-Ock,Hong, Jang-Hee,Seok, Jeong Ho,Lee, Choong Jae The Korean Academy of Tuberculosis and Respiratory 2013 Tuberculosis and Respiratory Diseases Vol.75 No.5
Background: We investigated whether prunetin significantly affects tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-induced MUC5AC mucin gene expression, production, inhibitory kappa B ($I{\kappa}B$) degradation and nuclear factor kappa B (NF-kB) 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 $I{\kappa}B$ and translocation of NF-${\kappa}B$ 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 $I{\kappa}B$ and translocation of NF-${\kappa}B$ p65. Conclusion: This result suggests that prunetin inhibits the NF-${\kappa}B$ signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production regulated by the NF-${\kappa}B$ signaling pathway.
( Jiho Ryu ),( Hyun Jae Lee ),( Su Hyun Park ),( Asaduzzaman Sikder ),( Ju Ock Kim ),( Jang Hee Hong ),( Jeong Ho Seok ),( Choong Jae Lee ) 대한결핵 및 호흡기학회 2013 Tuberculosis and Respiratory Diseases Vol.75 No.5
Background: We investigated whether prunetin significantly affects tumor necrosis factor-α (TNF-α)-induced MUC5AC mucin gene expression, production, inhibitory kappa B (IkB) degradation and nuclear factor kappa B (NF-kB) p65 translocation in human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with prunetin for 30 minutes and then stimulated with TNF-α 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-α-induced degradation of IkB and translocation of NF-κB 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-α. Prunetin inhibited TNF-α-induced degradation of IkB and translocation of NF-κB p65. Conclusion: This result suggests that prunetin inhibits the NF-κB signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production regulated by the NF-κB signaling pathway.
종양괴사인자로 유도된 기도 뮤신 생성, 뮤신 유전자 발현 및 NF-κB p65의 핵으로의 이동에 대한 크리신의 영향
신현대(Hyun-Dae Shin),박수현(Su Hyun Park),류지호(Jiho Ryu),무함마드 아사두자만 식더(Md. Asaduzzaman Sikder),이현재(Hyun Jae Lee),석정호(Jeong Ho Seok),이충재(Choong Jae Lee),홍장희(Jang-Hee Hong) 大韓藥學會 2012 약학회지 Vol.56 No.3
Chrysin and chlorogenic acid are natural products derived from Scutellariae Radix and Lonicerae Flos, respectively. We examined whether chrysin and chlorogenic acid affect airway mucin production induced by TNF-α in NCI-H292 cells. Cells were pretreated with each agent for 30 min and then stimulated with TNF-α for 24 h. Of the two compounds, chrysin suppressed airway MUC5AC mucin production. Also, chrysin suppressed MUC5AC mucin gene expression and translocation of NF-κB p65 induced by TNF-α. This result suggests that chrysin can regulate the production and gene expression of mucin induced by TNF-α through the inactivation of NF-κB in airway epithelial cells.