• YAKHAK HOEJI
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• v.54 no.5
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• pp.334-340
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• 2010

We investigated whether poly-L-histidine (PLH) significantly affect mucin release from cultured airway epithelial cells. Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled with $^$^3H$$glucosamine for 24 hr and chased for 30 min in the presence of PLH to assess the effect on $^3H$-mucin release. PLH 9,850 and PLH 6,700 specifically inhibit mucin release from airway goblet cells without significant cytotoxicity. This finding suggests that poly-L-histidine might function as an airway mucoregulative agent.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.6
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• pp.317-321
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• 2006

In this study, we investigated whether glycyrrhizin, prunetin and morroniside affect mucin secretion from cultured airway epithelial cells and compared the possible activities of these agents with the inhibitory action on mucin secretion by poly-L-lysine (PLL) and the stimulatory action by adenosine triphosphate (ATP). Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled using $^{3}H-glucosamine$ for 24 h and chased for 30 min in the presence of varying concentrations of each agent to assess the effects on $^{3}H-mucin$ secretion. The results were as follows: 1) glycyrrhizin and morroniside increased basal mucin secretion from airway; 2) prunetin did not affect basal mucin secretion; 3) glycyrrhizin did not inhibit ATP-induced mucin secretion. We conclude that glycyrrhizin and morroniside can increase basal mucin secretion, by directly acting on airway mucin-secreting cells and suggest that two compounds be further investigated for the possible use as mild expectorants during the treatment of inflammatory airway diseases.

• The Journal of Korean Medicine
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• v.29 no.3
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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.

• Biomolecules & Therapeutics
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• v.18 no.3
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• pp.294-299
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• 2010

In this study, we tried to investigate whether platycodin D significantly affects MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF), phorbol ester (PMA) and tumor necrosis factor-$\alpha$ (TNF-$\alpha$) from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of platycodin D for 30 min and then stimulated with EGF, PMA and TNF-$\alpha$ for 24h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) Platycodin D was found to inhibit the production of MUC5AC mucin protein induced by EGF, PMA, and TNF-$\alpha$, respectively. (2) It also inhibited the expression of MUC5AC mucin gene induced by the same inducers. These results suggest that platycodin D can regulate mucin gene expression and production of mucin protein, by directly acting on human airway epithelial cells.

• The Journal of Pediatrics of Korean Medicine
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• v.28 no.2
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• pp.56-71
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• 2014

Objectives In this study, the author tried to investigate whether piryongbang-gamgil-tang (PGGT) significantly affect in vitro airway mucin secretion, PMA- or EGF- or TNF-${\alpha}$-induced MUC5AC mucin production / gene expression from human airway epithelial cells and increase in airway epithelial mucosubstances and hyperplasia of tracheal goblet cells of rats. Materials and Methods For in vitro experiment, confluent RTSE cells were chased for 30 min in the presence of PGGT to assess the effect of PGGT on mucin secretion by enzyme-linked immunosorbent assay (ELISA). Also, effect of PGGT on PMA- or EGFor 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 PGGT and treated with PMA (10 ng/ml) or EGF (25 ng/ml) or TNF-${\alpha}$ (0.2 nM) for 24 hrs, to assess both effect of PGGT on PMA- or EGF- or TNF-${\alpha}$-induced MUC5AC mucin production by ELISA and gene expression by reverse transcription-polymerase chain reaction (RT-PCR). For in vivo experiment, the author induced hypersecretion of airway mucus and goblet cell hyperplasia by exposure of rats to $SO_2$ during 3 weeks. Effect of orally-administered PGGT during 2 weeks on increase in airway epithelial mucosubstances from tracheal goblet cells of rats and hyperplasia of goblet cells were assesed by using histopathological analysis after staining the epithelial tissue with alcian blue. Possible cytotoxicities of PGGT in vitro were assessed by examining LDH release from RTSE cells and the rate of survival and proliferation of NCI-H292 cells. In vivo liver and kidney toxicities of PGGT were evaluated by measuring serum GOT/GPT activities and serum BUN/creatinine concentrations of rats after administering PGGT orally. Results (1) PGGT did not affect in vitro mucin secretion from cultured RTSE cells. (2) PGGT significantly inhibited PMA-, EGF-, and TNF-${\alpha}$-induced MUC5AC mucin productions and the expression levels of MUC5AC mRNA from NCI-H292 cells. (3) PGGT decreased the amount of intraepithelial mucosubstances and showed the tendency of expectorating airway mucus already produced. (4) PGGT increased LDH release from RTSE cells. However, PGGT did not show in vivo liver and kidney toxicities and cytotoxicity to NCI-H292 cells. Conclusion The result from this study suggests that PGGT can regulate the production and gene expression of airway mucin observed in diverse respiratory diseases accompanied by mucus hypersecretion and do not show in vivo toxicity to liver and kidney functions after oral administration. Effect of PGGT with their components should be further studied using animal experimental models that reflect the diverse pathophysiology of respiratory diseases through future investigations.

• Biomolecules & Therapeutics
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• v.18 no.4
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• pp.396-401
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• 2010

We conducted this study to investigate whether baicalin, baicalein or schizandrin significantly affect MUC5AC mucin production induced by epidermal growth factor (EGF) or phorbol ester (PMA) in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of baicalin, baicalein or schizandrin for 30 min and then stimulated with EGF or PMA for 24 h, respectively. MUC5AC mucin protein production was measured by ELISA. The results were as follows: (1) Baicalin was found to inhibit the production of MUC5AC mucin protein induced by both EGF and PMA. (2) Baicalein, the aglycone of baicalin, also inhibited MUC5AC mucin production. (3) Schizandrin, derived from Schizandrae Fructus, inhibited MUC5AC mucin production by the same inducers. These results suggest that baicalin, baicalein and schizandrin can regulate the production of mucin protein by directly acting on human airway epithelial cells.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.3
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• pp.155-158
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• 2005

In this study, we investigated whether sphingosine-1-phosphate, furosemide, and indomethacin affect mucin release from airway goblet cells. Confluent primary hamster tracheal surface epithelial cells were metabolically radiolabeled and chased for 30 min or 24 hr in the presence of varying concentrations of the above agents to assess the effects on $^3H-mucin$ release. Sphingosine-1-phosphate stimulated mucin release during 30 min of treatment period in a dose-dependent manner. However, furosemide and indomethacin showed no effect on both basal and stimulated mucin release during 30 min or 24 hr of treatment period. We conclude that sphingosine-1-phosphate can affect mucin release by directly acting on airway mucin-secreting cells.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.6
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• pp.323-326
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• 2005

In the present study, we investigated whether ambroxol, S-carboxymethyl-L-cysteine, dextromethorphan and noscapine affect mucin release from airway goblet cells. Confluent primary hamster tracheal surface epithelial cells were metabolically radiolabeled and chased for 30 min in the presence of varying concentrations of the above agents to assess the effects on $^3H$-mucin release. Noscapine stimulated mucin release during 30 min of treatment period in a dose-dependent manner. However, ambroxol, S-carboxymethyl-L-cysteine and dextromethorphan showed no significant effect on mucin release during 30 min of treatment period. We conclude that noscapine can affect mucin release by acting on airway mucin-secreting cells.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.6
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• pp.329-333
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• 2004

In this study, we investigated whether TNF-alpha, IL-1beta, CTMA (carboxymethyl trimethylammonium) and LPD (Lup-20[29]-ene-3beta,28-diol) affect mucin release from airway goblet cells and compared the activities of these agents with the inhibitory action of PLL and the stimulatory action of ATP on mucin release. Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled with $^3H-glucosamine$ for 24 h and chased for 30 min in the presence of varying concentrations of each agent to assess the effects on $^3H-mucin$ release. The results were as follows: TNF-alpha, CTMA and LPD increased mucin release at the highest concentration, but IL-1beta did not. We conclude that CTMA and LPD can stimulate mucin release by directly acting on airway mucin-secreting cells, and suggest that these agents should be further investigated for the possible use as mild expectorants during the treatment of chronic airway diseases.

• Biomolecules & Therapeutics
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• v.14 no.4
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• pp.202-206
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• 2006

Angelicae Dahiricae Radix has been used for controlling inflammatory respiratory diseases in oriental medicine and their components, phellopterin, isoimperatorin and byakangelicol were reported to have various biological effects. In this study, we investigated whether phellopterin, isoimperatorin and byakangelicol affect adenosine triphosphate(ATP)-induced mucin secretion from cultured airway epithelial cells. Confluent primary hamster tracheal surface epithelial(HTSE) cells were metabolically radiolabeled using $^3H$-glucosamine for 24 h and chased for 30 min in the presence of varying concentrations of each agent to assess the effects on $^3H$-mucin secretion. The results were as follows: 1) phellopterin significantly inhibited ATP-induced mucin secretion; 2) However, isoimperatorin and byakangelicol did not affect ATP-induced mucin secretion, significantly. This result suggests that phellopterin can regulate 'mucin secretion induced by ATP'-a phenomenon simulating mucus overproduction from inflamed airway epithelial cells-by directly acting on airway mucin-secreting cells. Therefore, phellopterin should further be investigated for the possible use as mucoregulators in the treatment of inflammatory airway diseases.