• Biomolecules & Therapeutics
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• v.13 no.4
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• pp.251-255
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• 2005

In the present study, we tried to investigate whether protein kinase C (PKC) activator, phorbol 12-Myristate 13-Acetate (PMA), and PKC inhibitors, $G\"{o}-6976$, Ro-31-8220 and rottlerin significantly affect basal mucin relesed from cultured airway goblet 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 each agent to assess the effects on $^3H$-mucin release. The results were as follows: (1) PMA increased mucin release from cultured HTSE cells, during 30 min of treatment period; (2) However, $G\"{o}-6976$, Ro-31-8220 and rottlerin did not significantly affect mucin release, during 30 min of treatment period. This finding suggests, at least in part, that PKC might playa minor role in the signaling pathways involved in basal - physiological or constitutive - mucin release from airway goblet cells, although further studies are needed.

• Natural Product Sciences
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• v.25 no.3
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• pp.248-254
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• 2019

In the present study, we investigated whether quercitrin, quercetin and afzelin derived from Houttuynia cordata affect the production and gene expression of MUC5AC mucin from airway epithelial cells. Confluent NCI-H292 cells were pretreated with quercitrin, quercetin or afzelin for 30 min and then stimulated with epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA) for 24 h. The MUC5AC mucin gene expression and production were measured by RT-PCR and ELISA, respectively. The results were as follows: (1) Quercitrin, quercetin and afzelin inhibited EGF- and PMA-induced MUC5AC mucin production from NCI-H292 cells; (2) The three natural products also decreased EGF- and PMA-induced MUC5AC mucin gene expression in NCI-H292 cells. These results suggest that quercitrin, quercetin and afzelin showed the regulatory effect on the steps of gene expression and production of mucin, by directly acting on airway epithelial cells.

• The Journal of Korean Medicine
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• v.29 no.4
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• pp.123-132
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• 2008

Objective: In this study, the author tried to investigate whether revised Seonbangpaedok-tang (SPT) and Sigyeongcheongpye-tang (SCT) significantly effects both PMA-induced mucin production and MUC5AC gene expression from airway epithelial cells. Objective: In this study, the author tried to investigate whether revised Seonbangpaedok-tang (SPT) and Sigyeongcheongpye-tang (SCT) significantly affects both PMA-induced mucin production and MUC5AC gene expression from airway epithelial cells. Materials and Methods: Confluent NCI-H292 cells were pretreated for 30 min in the presence of SPT and SCT and treated with PMA (10 ng/$m{\ell}$), to assess the effects of the agents on PMA-induced mucin production by enzyme-linked immunosorbent assay (ELISA). Also, the effects of the agents on PMA-induced MUC5AC gene expression from the same cells were investigated. Possible cytotoxicities of the agent were assessed by measuring the rate of survival and proliferation of NCI-H292 cells after treatment of agents during 48 hrs. Results: (1) SPT and SCT did not show significant cytotoxicity to NCI-H292 cells; (2) SPT significantly inhibitedthe expression levels of PMA-induced MUC5AC gene in NCI-H292 cells. SCT slightly decreased the expression levels of PMA-induced MUC5AC gene; (3) SPT significantly decreased PMA-induced mucin production from NCI-H292 cells. However, SCT did not affect mucin production. Conclusion: Theseresults suggest that SPT can not only affect the production of mucin but also the expression of the mucin gene and this explains the traditional use of SPT in oriental medicine. The effects of SPT and SCT with their components should be further investigated using animal experimental models that reflect pathophysiology of airway diseases via ongoing studies.

• Tuberculosis and Respiratory Diseases
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• v.78 no.3
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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.

• Natural Product Sciences
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• v.21 no.1
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• pp.59-65
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• 2015

In this study, we investigated whether cynaroside, cynarin and linarin derived from Chrysanthemum indicum L. affect the secretion, production and gene expression of MUC5AC mucin in airway epithelial cells. Confluent NCI-H292 cells were pretreated with cynaroside, cynarin or linarin for 30 min and then stimulated with PMA (phorbol 12-myristate 13-acetate) for 24 h. The MUC5AC mucin gene expression, mucin protein production and secretion were measured by RT-PCR and ELISA, respectively. Effect of linarin on EGF (epidermal growth factor) - or TNF-${\alpha}$ (tumor necrosis factor-${\alpha}$)-induced MUC5AC mucin gene expression and mucin protein production was also examined. The results were as follows: (1) Cynaroside and cynarin did not significantly affect PMA-induced MUC5AC mucin secretion from NCI-H292 cells. However, linarin decreased MUC5AC mucin secretion; (2) Cynaroside did not affect PMA-induced MUC5AC mucin production and gene expresion from NCI-H292 cells. However, cynarin and linarin inhibited the production and gene expression of MUC5AC mucin; (3) Linarin also inhibited the production and gene expression of MUC5AC mucin induced by EGF- or TNF-${\alpha}$ from NCI-H292 cells. These results suggest that linarin can regulate the gene expression, production and secretion of mucin, by directly acting on airway epithelial cells.

• Natural Product Sciences
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• v.23 no.3
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• pp.201-207
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• 2017

Angelica decursiva has been utilised as remedy for controlling the airway inflammatory diseases in folk medicine. We investigated whether nodakenin, columbianadin, and umbelliferone isolated from the roots of Angelica decursiva inhibit the gene expression and production of MUC5AC mucin from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with nodakenin, columbianadin or umbelliferone for 30 min and then stimulated with epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) for 24 h. The MUC5AC mucin gene expression was measured by reverse transcription - polymerase chain reaction (RT-PCR). Production of MUC5AC mucin protein was measured by enzyme-linked immunosorbent assay (ELISA). The results were as follows: (1) Nodakenin did not affect the expression of MUC5AC mucin gene induced by EGF, PMA or $TNF-{\alpha}$. Columbianadin inhibited the expression of MUC5AC mucin gene induced by EGF or PMA. However, umbelliferone inhibited the expression of MUC5AC mucin gene induced by EGF, PMA or $TNF-{\alpha}$; (2) Nodakenin also did not affect the production of MUC5AC mucin protein induced by EGF, PMA or $TNF-{\alpha}$. Columbianadin inhibited the production of MUC5AC mucin protein induced by PMA. However, umbelliferone inhibited the production of MUC5AC mucin protein induced by EGF, PMA or $TNF-{\alpha}$. These results suggest that, among the three compounds investigated, umbelliferone only inhibits the gene expression and production of MUC5AC mucin stimulated by various inducers, by directly acting on airway epithelial cells, and the results might explain the traditional use of Angelica decursiva as remedy for diverse inflammatory pulmonary diseases.

• The Journal of Pediatrics of Korean Medicine
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• v.21 no.3
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• pp.33-55
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• 2007

Objectives In the present study, the author intended to investigate whether bojung-ikgitang-gamibang(BJGB) and seonbang-paedoktang(SBPT) significantly affect in vivo and in vitro mucin secretion from airway epithelial cells. Methods In vivo experiment, mice's mucin which is on a hypersecretion of airway mucin, mice's tracheal goblet cells in hyperplasia and mice's intraepithelial mucosubstances were exposed with SO2for3weeks. Effects of orally-administered BJGB and SBPT during 1 week on vivo mucin secretion and hyperplasia of tracheal goblet cells were assessed by using both enzyme-linked immunosorbent assay(ELISA) and staining goblet cells with alcian blue. In vitro experiment, confluent hamster tracheal surface epithelial(HTSE) cells were metabolically radiolabeled with 3H-glucosamine for 24hrs and chased for 30 min in the presence of each agent to figure out the effectiveness of 3H-mucin secretion. Total elution profiles of control spent media and treatment sample through Sepharose CL-4B column were analyzed. The effects of each agent on contractility of isolated tracheal smooth muscle and effects of each agent on MUC5AC gene expression in cultured HTSE cells were investigated. Also, possible cytotoxicities of each agent were assessed by measuring lactate dehydrogenase(LDH) release. Additionally, effects of BJGB and SBPT on both MUC5AC gene expression in cultured HTSE cells and TNF- or EGF-induced MUC5AC gene expression in human airway epithelial cells (NCI-H292) were investigated. Results (1) BJGB and SBPT inhibited hypersecretion of in vivo mucin. SBPT also inhibited the increase the number of goblet cells. However, BJGB did not affect the increase of number of goblet cells; (2) BJGB significantly increased mucin secretion from cultured HTSE cells, without significant cytotoxicity, and chiefly affected the 'mucin' secretion; (3) SBPT did not affect mucin secretion from cultured HTSE cells without significant cytotoxicity, and also did not affect the secretion of the other releseable glycoproteins; (4) BJGB and SBPT did not affect Ach-induced contraction of isolated tracheal smooth muscle; (5) SBPT significantly inhibit the expression levels of MUC5AC gene and BJGB significantly increased the expression levels of MUC5AC gene in both HTSE cells and NCI-H292 cells. Conclusions BJGB and SBPT can not only affect the secretion of mucin but also affect the expression of mucin gene. The author suggests that the effects BJGB and SBPT with their components should be further investigated and it is highly desirable to find from oriental medical prescriptions, novel agents which might regulate hypersecretion of mucin from airway epithelial cells.

• The Journal of Internal Korean Medicine
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• v.29 no.3
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• pp.765-777
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• 2008

Objectives : In this study, the author tried to examine whether Gamijinhae-tang and Socheongryong-tang-ga-seokgo significantly affect both PMA-induced mucin production and MUC5AC gene expression from airway epithelial cells. Materials and Methods : Confluent NCI-H292 cells were pretreated for 30 min in the presence of JHT and STS and treated with PMA (10ng/ml), to assess the effects of the agents on PMA-induced mucin production by enzyme-linked immunosorbent assay (ELISA). Also, the effects of the agents on PMA-induced MUC5AC gene expression from the same cells were investigated. Possible cytotoxicities of the agent were assessed by examining the rate of survival and proliferation of NCI-H292 cells after treatment of agents during 48 hrs. Results : (1) JHT and STS did not show significant cytotoxicity to NCI-H292 cells. (2) JHT significantly decreased PMA-induced mucin production from NCI-H292 cells. However. STS did not affect mucin production. (3) JHT significantly inhibit the expression levels of PMA-induced MUC5AC gene in NCI-H292 cells. STS slightly decreased the expression levels of PMA-induced MUC5AC gene. Conclusion : These results suggest that JHT can not only affect the production of mucin but also affect the expression of the mucin gene, and this explains the traditional use of JHT in oriental medicine. The effects of JHT and STS with their components should be further investigated using animal experimental models that simulate pathophysiology of airway diseases through future studies.

• Biomolecules & Therapeutics
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• v.14 no.3
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• pp.166-170
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• 2006

In this study, we investigated whether schizandrin, schizandrin-A, gomisin-A and uridine affect mucin secretion from cultured airway epithelial cells and compared the potential activities of these agents with the inhibitory action on mucin secretion by poly-1-lysine (PLL) and the stimulatory action by adenosine triphosphate (ATP). 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: schizandrin-A and uridine increased mucin secretion at the highest concentrations ($2{\times}10^{-4}\;-\;10^{-3}M$). We conclude that schizandrin-A and uridine can stimulate mucin secretion via direct effect on airway mucin-secreting cells and suggest that these agents be further investigated for the potential use as mucoregulators during the treatment of chronic airway diseases.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.5
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• pp.251-254
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• 2006

Schizandrae Fructus has been used for controlling respiratory allergic or inflammatory diseases in folk medicine and their components, schizandrin, schizandrin-A and gomisin-A were reported to have diverse biological effects. In this study, we investigated whether schizandrin, schizandrin-A and gomisin-A affect adenosine triphosphate (ATP)-induced mucin secretion from cultured airway epithelial cells. Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radio labeled 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) schizandrin significantly inhibited ATP-induced mucin secretion; 2) However, schizandrin-A and gomisin-A did not affect ATP-induced mucin secretion, significantly. We conclude that schizandrin can inhibit ATP-induced mucin secretion by directly acting on airway mucin-secreting cells. Therefore, schizandrin should further be investigated for the possible use as mucoregulators in the treatment of inflammatory airway diseases.