Production Of MUC5AC Mucin Protein Research Articles

인간 기도 상피세포에서 IKK/IκBα/NF-κB p65 신호전달 경로를 경유한 호흡기 MUC5AC 뮤신 유전자의 발현에 미치는 올레아놀산의 영향

In the present study, we investigated whether oleanolic acid, an anti-inflammatory natural product, significantly affects the phorbol 12-myristate 13-acetate (PMA)-induced gene expression of airway MUC5AC mucin. Confluent NCIH292 cells were pretreated with oleanolic acid for 30 min and then stimulated with PMA for 24 h or the indicated periods. The MUC5AC mucin mRNA expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. To elucidate the action mechanism of oleanolic acid, effect of oleanolic acid on PMA-induced NF-B signaling pathway was investigated by western blot analysis. The results were as follows: (1) Oleanolic acid significantly inhibited the production of MUC5AC mucin protein and down-regulated the expression of MUC5AC mucin mRNA; (2) Oleanolic acid inhibited PMA-induced activation (phosphorylation) of inhibitory kappa B kinase (IKK), and thus phosphorylation and degradation of inhibitory kappa Ba (IB); (3) Oleanolic acid inhibited PMA-induced nuclear translocation of nuclear factor kappa B (NF-B) p65, led to the down-regulation of MUC5AC mucin gene expression in NCI-H292 cells. These results suggest that oleanolic acid can regulate the gene expression of mucin by acting on airway epithelial cells through regulation of NF-B signaling pathway.

Effect of Paeoniae Radix Rubra (Paeonia lactiflora Pall.) extract on mucin secretion, gene expression in human airway epithelial cells

Ethnopharmacological relevancePaeoniae Radix Rubra (PRR), the root of Paeonia lactiflora Pall., is a traditional Chinese medicine which has the effects of regulating various inflammatory diseases, treating blood stasis, and enhancing blood circulation. Aim of the studyThis study examined whether Paeoniae Radix rubra extract (PRRE) and Paeoniflorin (PF) affect mucin production, gene expression including MUC5AC, and protein expression related to the ERK pathway induced by TNF-α from human airway epithelial cells. Materials and methodsNCI–H292 cells induced by TNF-α were treated with each agent. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction, staining, and enzyme-linked immunosorbent assay. Western blot was used to investigate the cell signaling pathways. ResultsPRRE and PF inhibited the production of MUC5AC mucin protein and gene expression in TNF-α-induced H292 cells. In Western blot, PRRE was involved in protein expression related to the ERK pathway. ConclusionsOverall, PRRE effectively inhibited the MUC5AC, and inflammatory cytokines expression caused by TNF-α, which was closely involved in the ERK pathway. PRRE may have the potential for treating mucus producing respiratory inflammation.

Effects of Natural Products Derived from Persicae Semen including Daucosterol on gene Expression and Production of Respiratory Mucin induced by Growth Factor and Phorbol Ester

Persicae semen was used as folk remedy for regulating pulmonary inflammatory diseases in traditional oriental medicine. In the prersent study, we investigated whether prunasin, erucic acid or daucosterol derived from Persicae semen affects airway MUC5AC mucin gene expression and production, induced by phorbol 12-myristate 13-acetate (PMA) or epi-dermal growth factor (EGF) from NCI-H292 cells. Confluent cells were pretreated with each agent for 30 min and then stim-ulated with PMA or EGF for 24h. The MUC5AC mucin gene expression was measured by RT-PCR (Reverse Transcription-Polymerase Chain Reaction). Production of MUC5AC mucin protein was measured by enzyme-linked immunosorbent assay (ELISA). The results were as follows: (1) Erucic acid inhibited the gene expression and production of MUC5AC mucin from NCI-H292 cells; (2) Daucosterol also inhibited the gene expression and production of MUC5AC mucin from NCI-H292 cells. This result suggests that erucic acid or daucosterol can inhibit the production and gene expression of mucin induced by PMA or EGF, through directly acting on airway epithelial cells.

Tussilagone suppressed the production and gene expression of MUC5AC mucin via regulating nuclear factor-kappa B signaling pathway in airway epithelial cells

In the present study, we investigated whether tussilagone, a natural product derived from Tussilago farfara, significantly affects the production and gene expression of airway MUC5AC mucin. Confluent NCI-H292 cells were pretreated with tussilagone for 30 min and then stimulated with EGF (epidermal growth factor) or PMA (phorbol 12-myristate 13-acetate) for 24 h or the indicated periods. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. To elucidate the action mechanism of tussilagone, effect of tussilagone on PMA-induced NF-κB signaling pathway was investigated by western blot analysis. Tussilagone significantly inhibited the production of MUC5AC mucin protein and down-regulated the expression of MUC5AC mucin gene, induced by EGF or PMA. Tussilagone inhibited PMA-induced activation (phosphorylation) of inhibitory kappa B kinase (IKK), and thus phosphorylation and degradation of inhibitory kappa Ba (IκBα). Tussilagone inhibited PMA-induced phosphorylation and nuclear translocation of nuclear factor kappa B (NF-κB) p65. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. These results suggest that tussilagone can regulate the production and gene expression of mucin by acting on airway epithelial cells through regulation of NF-κB signaling pathway.

Verticine, ebeiedine and suchengbeisine isolated from the bulbs of Fritillaria thunbergii Miq. inhibited the gene expression and production of MUC5AC mucin from human airway epithelial cells

BackgroundThe bulb of Fritillaria thunbergii has been utilised as mucoregulators and expectorants for controlling the airway inflammatory diseases in folk medicine. Hypothesis/PurposeWe investigated whether verticine, ebeiedine and suchengbeisine isolated from the bulbs of Fritillaria thunbergii inhibit the gene expression and production of MUC5AC mucin from human airway epithelial cells. Study designConfluent NCI-H292 cells were pretreated with verticine, ebeiedine or suchengbeisine for 30min and then stimulated with EGF, PMA or TNF-α for 24h. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. Results(1) Verticine, ebeiedine or suchengbeisine inhibited the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-α; (2) The production of MUC5AC mucin protein induced by EGF, PMA or TNF-α were also inhibited by treatment of verticine, ebeiedine or suchengbeisine. ConclusionThese results suggest that verticine, ebeiedine and suchengbeisine isolated from the bulbs of Fritillaria thunbergii inhibit the gene expression and production of MUC5AC mucin, by directly acting on airway epithelial cells, and the results are consistent with the traditional use of Fritillaria thunbergii as remedy for diverse inflammatory pulmonary diseases.

Dioscin and methylprotodioscin isolated from the root of Asparagus cochinchinensis suppressed the gene expression and production of airway MUC5AC mucin induced by phorbol ester and growth factor

BackgroundThe root of Asparagus cochinchinensis (Lour.) Merr. has been utilized as mucoregulators and expectorants for controlling the airway inflammatory diseases in folk medicine. Hypothesis/purposeWe investigated whether dioscin and methylprotodioscin isolated from the root of Asparagus cochinchinensis (Lour.) Merr. suppress the gene expression and production of airway MUC5AC mucin induced by phorbol ester and growth factor. Study designConfluent NCI-H292 cells were pretreated with dioscin or methylprotodioscin for 30 min and then stimulated with EGF or PMA for 24 h. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. Results(1) Dioscin and methylprotodioscin suppressed the expression of MUC5AC mucin gene induced by EGF or PMA; (2) dioscin suppressed the production of MUC5AC mucin induced by either EGF at 10−5 M (p < 0.05) and 10−6 M (p < 0.05) or PMA at 10−4 M (p < 0.05), 10−5 M (p < 0.05) and 10−6 M (p < 0.05); (3) methylprotodioscin also suppressed the production of MUC5AC mucin induced by either EGF at 10−4 M (p < 0.05) or PMA at 10−4 M (p < 0.05). ConclusionThese results suggest that dioscin and methylprotodioscin isolated from the root of Asparagus cochinchinensis suppress the gene expression and production of MUC5AC mucin, by directly acting on airway epithelial cells, and the results are consistent with the traditional use of Asparagus cochinchinensis as remedy for diverse inflammatory pulmonary diseases.

Luteolin inhibited the gene expression, production and secretion of MUC5AC mucin via regulation of nuclear factor kappa B signaling pathway in human airway epithelial cells

Luteolin, a flavonoidal compound derived from Lonicera japonica Thunb. and Chrysanthemum indicum L., has been reported to show anti-inflammatory, anti-oxidative and anti-carcinogenic effects. In this study, we investigated whether luteolin significantly affects the secretion, production and gene expression of airway mucin. Confluent NCI-H292 cells were pretreated with luteolin for 30 min and then stimulated with EGF (epidermal growth factor) or PMA (phorbol 12-myristate 13-acetate) for 24 h or the indicated periods. The MUC5AC mucin gene expression was measured by RT-PCR. Production and secretion of MUC5AC mucin protein were measured by ELISA. To elucidate the action mechanism of luteolin, effect of luteolin on PMA-induced NF-κB signaling pathway was investigated by western blot analysis. The results were as follows: (1) Luteolin inhibited the secretion of MUC5AC mucin protein induced by EGF or PMA; (2) Luteolin inhibited the production of MUC5AC mucin protein and the expression of MUC5AC mucin gene induced by EGF or PMA; (3) Luteolin inhibited PMA-induced phosphorylation and degradation of inhibitory kappa Bα (IκBα); (4) Luteolin inhibited PMA-induced phosphorylation and nuclear translocation of nuclear factor kappa B (NF-κB) p65. This result suggests that luteolin can regulate the secretion, production and gene expression of mucin by acting on airway epithelial cells via regulation of NF-kB signaling pathway.

Suppressive effects of coixol, glyceryl trilinoleate and natural products derived from Coix Lachryma-Jobi var. ma-yuen on gene expression, production and secretion of airway MUC5AC mucin.

In this study, we investigated whether natural products including coixol derived from Coix Lachryma-Jobi var. ma-yuen affect MUC5AC mucin gene expression, production and secretion from airway epithelial cells. Confluent NCI-H292 cells were pretreated with oleic acid, linoleic acid, glyceryl trilinoleate, beta-stigmasterol or coixol for 30min and then stimulated with PMA (phorbol 12-myristate 13-acetate), EGF (epidermal growth factor) or TNF-α (tumor necrosis factor-α) for 24h.The MUC5AC mucin gene expression, mucin protein production and secretion were measured by RT-PCR and ELISA. The results were as follows: (1) Oleic acid, linoleic acid, glyceryl trilinoleate, beta-stigmasterol and coixol inhibited the expression of MUC5AC mucin gene induced by PMA from NCI-H292 cells; (2) Oleic acid, linoleic acid, glyceryl trilinoleate, beta-stigmasterol and coixol also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells; (3) Coixol inhibited the expression of MUC5AC mucin gene and production of MUC5AC mucin protein, induced by EGF or TNF-α from NCI-H292 cells; (4) Coixol decreased PMA-induced MUC5AC mucin secretion from NCI-H292 cells. This result suggests that coixol, the characteristic component among the examined five natural products derived from C. Lachryma-Jobi var. ma-yuen, can regulate gene expression, production and secretion of mucin, by directly acting on airway epithelial cells.

Phorbol Ester or Epidermal Growth‐factor‐induced MUC5AC Mucin Gene Expression and Production from Airway Epithelial Cells are Inhibited by Apigenin and Wogonin

In this study, we investigated whether apigenin and wogonin affect 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. Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with PMA or EGF for 24 h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay (ELISA). The results were as follows: (i) apigenin and wogonin were found to inhibit the production of MUC5AC mucin protein induced by PMA or EGF; (ii) both compounds also inhibited the expression of MUC5AC mucin gene induced by PMA or EGF. These results suggest that apigenin and wogonin can inhibit mucin gene expression and production of mucin protein, by directly acting on airway epithelial cells.

Silibinin Regulates Gene Expression, Production and Secretion of Mucin from Cultured Airway Epithelial Cells

We investigated whether silibinin significantly affects gene expression, production and secretion of mucin from cultured airway epithelial cells. Confluent NCI-H292 cells were pretreated with silibinin for 30 min and then stimulated with epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or TNF-α for 24 h. 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). The effect of silibinin on TNF-α-induced activation of NF-κB p65 was also examined. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then treated for 30 min in the presence of silibinin to assess the effect on mucin secretion using ELISA. The results were as follows: (i) silibinin inhibited the expression of the MUC5AC mucin gene induced by EGF, PMA or TNF-α from NCI-H292 cells; (ii) silibinin also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells; (iii) silibinin inhibited the activation of NF-κB p65 by TNF-α in NCI-H292 cells; (iv) silibinin significantly decreased ATP-induced mucin secretion from cultured RTSE cells. This result suggests that silibinin can regulate gene expression, production and secretion of mucin by directly acting on airway epithelial cells.

Effect of Chrysin on Gene Expression and Production of MUC5AC Mucin from Cultured Airway Epithelial Cells

BackgroundWe 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.MethodsConfluent 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.ResultsConcentrations 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.ConclusionThese results suggest that chrysin can inhibit mucin gene expression and the production of mucin protein by directly acting on airway epithelial cells.

Resveratrol Inhibits Mucin Gene Expression, Production and Secretion From Airway Epithelial Cells

The study investigated whether resveratrol significantly affects mucin gene expression, production and secretion from airway epithelial cells. Confluent NCI-H292 cells were pretreated with resveratrol for 30 min and then stimulated with EGF (epidermal growth factor), PMA (phorbol 12-myristate 13-acetate) and TNF-α (tumor necrosis factor-α) for 24 h, respectively. The MUC5AC gene expression and mucin protein production were measured by RT-PCR and ELISA. The effect of resveratrol on TNF-α- or PMA-induced activation of NF-κB p65 was also examined. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then treated for 30 min in the presence of resveratrol to assess the effect on mucin secretion using ELISA. The results were as follows: (1) resveratrol inhibited the expression of MUC5AC gene induced by EGF or PMA or TNF-α from NCI-H292 cells; (2) resveratrol also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells; (3) resveratrol inhibited the activation of NF-κB p65 by TNF-α or PMA in NCI-H292 cells; (4) resveratrol significantly decreased ATP-induced mucin secretion from cultured RTSE cells. This result suggests that resveratrol can regulate mucin gene expression, production and secretion, by directly acting on airway epithelial cells.

Oleanolic Acid and Ursolic Acid Derived fromCornus officinalisSieb. et Zucc. Suppress Epidermal Growth Factor- and Phorbol Ester-induced MUC5AC Mucin Production and Gene Expression from Human Airway Epithelial Cells

In this study, the effects of oleanolic acid and ursolic acid on MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF) and phorbol 12-myristate 13-acetate (PMA) from human airway epithelial cells were investigated. Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with EGF and PMA for 24 h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. Oleanolic acid and ursolic acid were found to inhibit the production of MUC5AC mucin protein induced by EGF and PMA, and both compounds also inhibited the expression of MUC5AC mucin gene induced by EGF and PMA. These results suggest that oleanolic acid and ursolic acid can regulate mucin gene expression, and production of mucin protein, by directly acting on airway epithelial cells.

Inhibition of Secretion, Production and Gene Expression of Mucin from Cultured Airway Epithelial Cells by Prunetin

This study investigated whether prunetin significantly affects the secretion, production and gene expression of mucin from cultured airway epithelial cells. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then chased for 30 min in the presence of prunetin to assess the effect on mucin secretion using enzyme-linked immunosorbent assay (ELISA). At the same time, confluent NCI-H292 cells were pretreated with prunetin for 30 min and then stimulated with epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA) for 24 h, respectively. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction (RT-PCR) and ELISA. The results were as follows: (1) prunetin significantly suppressed ATP-induced mucin secretion from cultured RTSE cells; (2) prunetin inhibited the production of MUC5AC mucin protein induced by EGF or PMA from NCI-H292 cells; (3) prunetin also inhibited the expression of MUC5AC mucin gene induced by EGF or PMA from NCI-H292 cells. This result suggests that prunetin can regulate the secretion, production and gene expression of mucin, by directly acting on airway epithelial cells.

Effect of Ambroxol on Secretion, Production and Gene Expression of Mucin from Cultured Airway Epithelial Cells

In this study, we investigated whether ambroxol significantly affects secretion, production and gene expression of mucin from cultured airway epithelial cells. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then treated for 30 min with ambroxol to assess the effect on mucin secretion using ELISA. Additionally, confluent NCI-H292 cells were pretreated with ambroxol for 30 min and then stimulated with EGF or PMA 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) ambroxol did not significantly affect ATP-induced mucin secretion from cultured RTSE cells; (2) ambroxol inhibited the production of MUC5AC mucin protein induced by EGF and PMA in NCI-H292 cells; (3) ambroxol also inhibited the expression of MUC5AC mucin gene induced by EGF and PMA in NCI-H292 cells. This result suggests that ambroxol can inhibit the production and gene expression of MUC5AC mucin, by directly acting on human airway epithelial cells.

Inhibition of airway MUC5AC mucin production and gene expression induced by epidermal growth factor or phorbol ester by glycyrrhizin and carbenoxolone

In this study, we investigated whether glycyrrhizin and carbenoxolone affect MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF) or phorbol ester (PMA) from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with EGF and PMA for 24h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. Glycyrrhizin and carbenoxolone were found to inhibit the production of MUC5AC mucin protein induced by EGF or PMA, and both compounds also inhibited the expression of MUC5AC mucin gene induced by EGF or PMA. These results suggest that glycyrrhizin and carbenoxolone can inhibit mucin gene expression and production of mucin protein, by directly acting on airway epithelial cells.

Effects of Baicalin, Baicalein and Schizandrin on Airway Mucin Production Induced by Epidermal Growth Factor and Phorbol Ester

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.

Daidzein regulates secretion, production and gene expression of mucin from airway epithelial cells stimulated by proinflammatory factor and growth factor

In this study, we investigated whether daidzein significantly affects secretion, production and gene expression of mucin from cultured airway epithelial cells. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then chased for 30 min in the presence of daidzein to assess the effect on mucin secretion using ELISA. At the same time, confluent NCI-H292 cells were pretreated with daidzein for 30 min and then stimulated with EGF and PMA for 24 h, respectively. The MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) daidzein significantly decreased ATP-induced mucin secretion from cultured RTSE cells; (2) daidzein inhibited the production of MUC5AC mucin protein induced by EGF or PMA from NCI-H292 cells; (3) daidzein also inhibited the expression of MUC5AC mucin gene induced by EGF or PMA from NCI-H292 cells. This result suggests that daidzein can regulate secretion, production and gene expression of mucin, by directly acting on airway epithelial cells.

Effect of Platycodin D on Airway MUC5AC Mucin Production and Gene Expression Induced by Growth Factor and Proinflammatory Factor

Abstract － 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-α (TNF-α) 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-α 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-α, 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. Keywords: Airway mucin, MUC5AC, Platycodin D INTRODUCTION Airway mucus is very important in defensive action against invading pathogenic microorganisms, chemicals and particles. This defensive action of airway mucus is at-tributed to the physicochemical property of mucins i.e. viscoelasticity. Mucins are multimillion dalton glycoproteins present in the airway mucus and produced by goblet cells in the surface epithelium as well as mucous cells in the submucosal gland. However, hypersecretion of airway mu-cus is one of the major symptoms associated with severe pulmonary diseases including asthma, chronic bronchitis, cystic fibrosis and bronchiectasis (Ellis, 1985). Therefore, we suggest it is valuable to find the potential activity of reg-ulating (inhibiting) the excess mucin secretion (production) by the compounds derived from various medicinal plants. We have tried to investigate the possible activities of some natural products on mucin secretion from cultured airway epithelial cells. As a result of our trial, we previously re-ported that several natural compounds affected mucin se-cretion and/or production from airway epithelial cells (Lee

Regulation of Tumor Necrosis Factor-α-induced Airway Mucin Production and Gene Expression by Carbenoxolone, Prunetin, and Silibinin

Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-α-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-α for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Results: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-α; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-α. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-α, by directly acting on airway epithelial cells.