• 제목/요약/키워드: muc gene

검색결과 87건 처리시간 0.087초

Effect of Chrysin on Gene Expression and Production of MUC5AC Mucin from Cultured 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
    • Tuberculosis and Respiratory Diseases
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    • 제73권4호
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    • pp.204-209
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    • 2012
  • 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.

Effect of Geonpye-tang(GPT) on Production and Gene Expression of Respiratory Mucin (건폐탕(健肺陽)이 호흡기 뮤신의 생성 및 유전자 발현에 미치는 영향)

  • Jung, Byeong-Jin;Kim, Ho;Seo, Un-Kyo
    • The Journal of Internal Korean Medicine
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    • 제30권4호
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    • pp.685-695
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    • 2009
  • Objectives : In this study, the author tried to investigate whether Geonpye-tang(GPT) significantly affects PMA-, EGF- or TNF-alpha-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Materials and Methods : Effects of the agent on PMA-, EGF- or TNF-alpha-induced MUC5AC mucin production and gene expression from human airway epithelial cells (NCI-H292) were investigated. Confluent NCI-H292 cells were pretreated for 30 min in the presence of GPT and treated with PMA (10ng/ml) or EGF (25ng/ml) or TNF-alpha (0.2nM), to assess both effect of the agent on PMA- or EGF- or TNF-alpha-induced MUC5AC mucin production by enzyme-linked immunosorbent assay (ELISA) and gene expression by reverse transcription-polymerase chain reaction (RT-PCR). Possible cytotoxicity of the agent was assessed by examining the rate of survival and proliferation of NCI-H292 cells after treatment with the agent over 72 hrs (SRB assay). Results : (1) GPT significantly inhibited PMA-induced and EGF-induced MUC5AC mucin production from NCI-H292 cells. However, GPT did not affect TNF-alpha-induced MUC5AC mucin production. (2) GPT significantly inhibited the expression levels of PMA-, EGF- or TNF-alpha-induced MUC5AC genes in NCI-H292 cells (3) GPT did not show significant cytotoxicity to NCI-H292 cells. Conclusion : This result suggests that GPT can affect the production and gene expression of respiratory mucin observed in diverse respiratory diseases accompanied by mucus hypersecretion. This can explain the traditional use of GPT in oriental medicine. Effects of GPT with their components should be further investigated using animal experimental models that reflect pathophysiology of airway diseases through future studies.

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Pyunkang-hwan (Pyunkang-tang) Regulates Hypersecretion of Pulmonary Mucin from Rats with Sulfur Dioxide-Induced Bronchitis and Production and Gene Expression of MUC5AC Mucin from Human Airway Epithelial Cells

  • Seo, Hyo-Seok;Lee, Hyun Jae;Lee, Choong Jae
    • Natural Product Sciences
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    • 제20권3호
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    • pp.196-201
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    • 2014
  • Pyunkang-hwan (Pyunkang-tang) extract (PGT) is a traditional folk medicine for controlling diverse pulmonary diseases including bronchitis, tonsiltis and pneumonitis. We investigated whether PGT significantly affects secretion, production and gene expression of airway mucin using in vivo and in vitro experimental models reflecting the hypersecretion and/or hyperproduction of mucus observed in inflammatory pulmonary diseases. For in vivo experiment, effect of PGT was checked on hypersecretion of pulmonary mucin in sulfur dioxide-induced bronchitis in rats. For in vitro experiment, confluent NCI-H292 cells were pretreated with PGT for 30 min and then stimulated with EGF (epidermal growth factor), PMA (phorbol 12-myristate 13-acetate) or TNF-${\alpha}$ (tumor necrosis factor-${\alpha}$) for 24 h. The MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) PGT inhibited the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-${\alpha}$ from NCI-H292 cells, respectively; (2) PGT also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells, respectively; (3) PGT inhibited secretion of mucin in sulfur dioxide-induced bronchitis rat model. This result suggests that PGT can regulate secretion, production and gene expression of airway mucin.

Common Genetic Variations in the MUC5AC Gene are Not Related to Helicobacter pylori Serologic Status

  • Zhou, Cheng-Jiang;Zhang, Liu-Wei;Gao, Fang;Zhang, Bin;Wang, Ying;Chen, Da-Fang;Jia, Yan-Bin
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권24호
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    • pp.10719-10722
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    • 2015
  • Several lines of evidence suggest that MUC5AC genetic polymorphisms might confer susceptibility to H. pylori infection and therefore gastric cancer risk. We here assessed the association of common polymorphisms in the MUC5AC gene with H. pylori seroprevalence using an LD-based tagSNP approach in a north-western Chinese Han population. A total of 12 tagSNPs were successfully genotyped among 281 unrelated ethnic Han Chinese who had no cancer history, and no identifiable gastric disease or genetic disease. No significant association between any alleles, genotypes or haplotypes and H. pylori seroprevalence was observed. Our results suggest that common genetic variations in MUC5AC gene might not make a major contribution to the risk of H. pylori infection.

Effects of Inhibiting Glycoprotein MUC5AC by Seaweed Ecklonia cava Extract in human Airway Epithelial Cells

  • Lee, Sung-Gyu;Kwon, Sang-Oh
    • Biomedical Science Letters
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    • 제27권4호
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    • pp.334-339
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    • 2021
  • In the present study, antioxidant and MUC5AC mucin inhibition activities were measured in Ecklonia cava (E. cava) extract. The E. cava extract showed the total polyphenol and flavonoid contents of 607.40±19.44 ㎍ GAE/mg and 13.33±5.28 ㎍ QE/mg, respectively. The free radical scavenging activity of E. cava extract was high in the DPPH radical scavenging activity (RC50 7.08 ㎍/mL) and ABTS+ radical scavenging activity (RC50 4.74 ㎍/mL). Also, we investigated whether E. cava extract affects airway MUC5AC mucin gene expression, production and secretion induced by phorbol 12-myristate 13-acetate (PMA) from NCI-H292 cells. Cells were treated with E. cava extract and then stimulated with PMA for 24 h. The E. cava extract inhibited the gene expression of MUC5AC mucin from NCI-H292 cells. This result suggests that E. cava extract can inhibit the gene expression of mucin induced by PMA through directly acting on airway epithelial cells.

Effects of Haengso-tang and Chwiyeon-tang on Expression of Respiratory Mucin Gene and Secretion of Airway Mucus (행소탕(杏蘇湯) 및 취연탕(取淵湯)이 호흡기 뮤신 유전자의 발현과 점액분비에 미치는 영향)

  • Kang, Won-Je;Seo, Un-Kyo
    • The Journal of Korean Medicine
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    • 제29권3호
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    • pp.76-87
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    • 2008
  • Objectives: In this study, the author investigated whether Haengso-tang (HST) and Chwiyeon-tang (CHT) affect both in vitro mucin secretion and MUC5AC gene expression in airway epithelial cells and in vivo mucin secretion from animal model for airway mucus hypersecretion. Materials and Methods: Confluent HTSE cells (non-labeled) were chased for 30 min in the presence of HST and CHT to assess the effects of the agents on mucin secretion by enzyme-linked immunosorbent assay (ELISA), with removal of oriental herbal medicine extract from each agent-treated sample by centrifuge microfilter. Also, the effects of the agents on TNF- or EGF-induced MUC5AC gene expression in human airway epithelial cells (NCI-H292) were investigated. The author also induced hypersecretion of airway mucus by exposure of rats to SO2 for 3 weeks. Effects of orally-administered HST and CHT during 1 week on in vivo mucin secretion from tracheal goblet cells of rats were assessed using ELISA. Results: (1) HST significantly decreased in vitro mucin secretion from cultured HTSE cells. However, CHT did not affect in vitro mucin secretion from HTSE cells; (2) CHT significantly inhibited the expression levels of EGF- or TNF-alpha-induced MUC5AC gene in NCI-H292 cells. However, HST did not affect the expression levels of EGF- or TNF-alpha-induced MUC5AC gene in NCI-H292 cells; (3) CHT significantly inhibited hypersecretion of in vivo mucin. However, HST did not affect hypersecretion of in vivo mucin. Conclusion: These results suggest that CHT can not only affect the secretion of mucin but also the expression of the mucin gene and could be helpful for treating pulmonary disease caused by secretion of mucin.

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Betulin, an Anti-Inflammatory Triterpenoid Compound, Regulates MUC5AC Mucin Gene Expression through NF-kB Signaling in Human Airway Epithelial Cells

  • Hossain, Rajib;Kim, Kyung-il;Jin, Fengri;Lee, Hyun Jae;Lee, Choong Jae
    • Biomolecules & Therapeutics
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    • 제30권6호
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    • pp.540-545
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    • 2022
  • Betulin is a triterpenoid natural product contained in several medicinal plants including Betulae Cortex. These medicinal plants have been used for controlling diverse inflammatory diseases in folk medicine and betulin showed anti-inflammatory, antioxidative, and anticancer activities. In this study, we tried to examine whether betulin exerts a regulative effect on the gene expression of MUC5AC mucin under the status simulating a pulmonary inflammation, in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with betulin for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h or the indicated periods. The MUC5AC mucin mRNA expression and mucin glycoprotein production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. To elucidate the action mechanism of betulin, effect of betulin on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated by western blot analysis. The results were as follows: 1) Betulin significantly suppressed the production of MUC5AC mucin glycoprotein and down-regulated MUC5AC mRNA expression induced by PMA in NCI-H292 cells. 2) Betulin inhibited NF-κB activation stimulated by PMA. Suppression of inhibitory kappa B kinase (IKK) by betulin led to the inhibition of the phosphorylation and degradation of inhibitory kappa B alpha (IκBα), and the nuclear translocation of NF-κB p65. This, in turn, led to the down-regulation of MUC5AC glycoprotein production in NCI-H292 cells. These results suggest betulin inhibits the gene expression of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.

Diclofenac Inhibits Phorbol Ester-Induced Gene Expression and Production of MUC5AC Mucin via Affecting Degradation of IkBα and Translocation of NF-kB p65 in NCI-H292 Cells

  • Jin, Fengri;Li, Xin;Lee, Hyun Jae;Lee, Choong Jae
    • Biomolecules & Therapeutics
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    • 제28권5호
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    • pp.431-436
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    • 2020
  • In this study, diclofenac, a non-steroidal anti-inflammatory drug, was investigated for its potential effect on the gene expression and production of airway MUC5AC mucin. The human respiratory epithelial NCI-H292 cells were pretreated with diclofenac for 30 min and stimulated with phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect of diclofenac on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated. Diclofenac suppressed the production and gene expression of MUC5AC mucins, induced by PMA through the inhibition of degradation of inhibitory kappa Bα (IkBα) and NF-kB p65 nuclear translocation. These results suggest diclofenac regulates the gene expression and production of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.

Effects of Caffeic Acid, Myristicin and Rosemarinic Acid on the Gene Expression and Production of Airway MUC5AC Mucin

  • Lee, Hyun Jae;Lee, Kang Ro;Hong, Jang-Hee;Lee, Choong Jae
    • Natural Product Sciences
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    • 제22권4호
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    • pp.275-281
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    • 2016
  • Perilla frutescens was empirically used for controlling airway inflammatory diseases in folk medicine. We investigated whether caffeic acid, myristicin and rosemarinic acid derived from Perilla frutescens significantly affect the gene expression and production of mucin from airway epithelial cells. Confluent NCI-H292 cells were pretreated with caffeic acid, myristicin or rosemarinic acid for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h. The MUC5AC mucin gene expression and production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Additionally, we examined whether caffeic acid, myristicin or rosemarinic acid affects MUC5AC mucin production indued by epidermal growth factor (EGF) and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), the other two stimulators of production of airway mucin. The results were as follows: (1) Caffeic acid, myristicin and rosemarinic acid inhibited the gene expression and production of MUC5AC mucin induced by PMA from NCI-H292 cells, respectively; (2) Among the three compounds derived from Perilla frutescens, only rosemarinic acid inhibited the production of MUC5AC mucin induced by EGF or $TNF-{\alpha}$, the other two stimulators of production of airway mucin. These results suggest that rosemarinic acid derived from Perilla frutescens can regulate the production and gene expression of mucin, by directly acting on airway epithelial cells and, at least in part, explains the traditional use of Perilla frutescens as remedies for diverse inflammatory pulmonary diseases.

Effects of Lupenone, Lupeol, and Taraxerol Derived from Adenophora triphylla on the Gene Expression and Production of Airway MUC5AC Mucin

  • Yoon, Yong Pill;Lee, Hyun Jae;Lee, Dong-Ung;Lee, Sang Kook;Hong, Jang-Hee;Lee, Choong Jae
    • Tuberculosis and Respiratory Diseases
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    • 제78권3호
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    • pp.210-217
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    • 2015
  • Background: Adenophora triphylla var. japonica is empirically used for controlling airway inflammatory diseases in folk medicine. We evaluated the gene expression and production of mucin from airway epithelial cells in response to lupenone, lupeol and taraxerol derived from Adenophora triphylla var. japonica. Methods: Confluent NCI-H292 cells were pretreated with lupenone, lupeol or taraxerol for 30 minutes and then stimulated with tumor necrosis factor ${\alpha}$ (TNF-${\alpha}$) for 24 hours. The MUC5AC mucin gene expression and production were measured by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Additionally, we examined whether lupenone, lupeol or taraxerol affects MUC5AC mucin production induced by epidermal growth factor (EGF) and phorbol 12-myristate 13-acetate (PMA), the other 2 stimulators of airway mucin production. Results: Lupenone, lupeol, and taraxerol inhibited the gene expression and production of MUC5AC mucin induced by TNF-${\alpha}$ from NCI-H292 cells, respectively. The 3 compounds inhibited the EGF or PMA-induced production of MUC5AC mucin in NCI-H292 cells. Conclusion: These results indicated that lupenone, lupeol and taraxerol derived from Adenophora triphylla var. japonica regulates the production and gene expression of mucin, by directly acting on airway epithelial cells. In addition, the results partly explain the mechanism of of Adenophora triphylla var. japonica as a traditional remedy for diverse inflammatory pulmonary diseases.