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

Yoon YP, Lee HJ, Lee DU, Lee SK, Hong JH, Lee CJ - Tuberc Respir Dis (Seoul) (2015)

Bottom Line: Lupenone, lupeol, and taraxerol inhibited the gene expression and production of MUC5AC mucin induced by TNF-α from NCI-H292 cells, respectively.The 3 compounds inhibited the EGF or PMA-induced production of MUC5AC mucin in NCI-H292 cells.In addition, the results partly explain the mechanism of of Adenophora triphylla var. japonica as a traditional remedy for diverse inflammatory pulmonary diseases.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Chungnam National University School of Medicine, Daejeon, Korea.

ABSTRACT

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 α (TNF-α) 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-α 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.

No MeSH data available.


Related in: MedlinePlus

Chemical structure of lupenone (A), lupeol (B), and taraxerol (C).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4499588&req=5

Figure 1: Chemical structure of lupenone (A), lupeol (B), and taraxerol (C).

Mentions: All the chemicals and reagents used in this experiment were purchased from Sigma (St. Louis, MO, USA) unless otherwise specified. Lupenone (purity, 98.0%), lupeol (purity, 98.0%), and taraxerol (purity, 98.0%) (Figure 1) were isolated, purified and identified by analytical chemists in the Laboratory of Natural Product Science, Division of Bioscience, Dongguk University (Gyeongju, Korea). Briefly, roots of Adenophora triphylla var. japonica (cultivated in Jeongsun-gun, Gangwon-do, Korea) were provided and authenticated by Professor Je-Hyun Lee (College of Oriental Medicine, Dongguk University, Korea). Air-dried and chopped roots (300 g) were extracted with each of distilled water and 70% ethanol twice at 95℃ for 3 hours. The combined extracts were filtered and concentrated under reduced pressure to give 31.1 g (10.7%) and 38.4 g (12.8%) of crude extracts, respectively. In order to isolate its active constituents the ethanol extract was suspended in distilled water, then consecutively partitioned with organic solvents to give the corresponding hexane (3.6 g), dichloromethane (0.23 g), ethylacetate (0.09 g), and n-butanol (1.4 g) fractions. The main hexane fraction was subjected to column chromatographic separation on a silica gel column using a stepwise elution with dichloromethane, dichloromethane-MeOH 50:1, and dichloromethane-MeOH 1:1 to yield fractions F1-F12. Fraction F3 was recrystallized with dichloromethane-EtOH (two-phase system) 1:1 to give taraxerol (10.8 mg, 0.3%). Fraction F7 was further chromatographed with dichloromethane to afford five subfractions SF1-SF5. Among the subfractions, SF5 was separated by silica gel column chromatography using dichloromethane and MeOH (10:1 to 1:1 gradient) to furnish lupenone (136.8 mg, 3.8%) and lupeol (28.8 mg, 0.8%). The isolated compounds were identified by comparison of their spectral data with literature values141516.


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

Yoon YP, Lee HJ, Lee DU, Lee SK, Hong JH, Lee CJ - Tuberc Respir Dis (Seoul) (2015)

Chemical structure of lupenone (A), lupeol (B), and taraxerol (C).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4499588&req=5

Figure 1: Chemical structure of lupenone (A), lupeol (B), and taraxerol (C).
Mentions: All the chemicals and reagents used in this experiment were purchased from Sigma (St. Louis, MO, USA) unless otherwise specified. Lupenone (purity, 98.0%), lupeol (purity, 98.0%), and taraxerol (purity, 98.0%) (Figure 1) were isolated, purified and identified by analytical chemists in the Laboratory of Natural Product Science, Division of Bioscience, Dongguk University (Gyeongju, Korea). Briefly, roots of Adenophora triphylla var. japonica (cultivated in Jeongsun-gun, Gangwon-do, Korea) were provided and authenticated by Professor Je-Hyun Lee (College of Oriental Medicine, Dongguk University, Korea). Air-dried and chopped roots (300 g) were extracted with each of distilled water and 70% ethanol twice at 95℃ for 3 hours. The combined extracts were filtered and concentrated under reduced pressure to give 31.1 g (10.7%) and 38.4 g (12.8%) of crude extracts, respectively. In order to isolate its active constituents the ethanol extract was suspended in distilled water, then consecutively partitioned with organic solvents to give the corresponding hexane (3.6 g), dichloromethane (0.23 g), ethylacetate (0.09 g), and n-butanol (1.4 g) fractions. The main hexane fraction was subjected to column chromatographic separation on a silica gel column using a stepwise elution with dichloromethane, dichloromethane-MeOH 50:1, and dichloromethane-MeOH 1:1 to yield fractions F1-F12. Fraction F3 was recrystallized with dichloromethane-EtOH (two-phase system) 1:1 to give taraxerol (10.8 mg, 0.3%). Fraction F7 was further chromatographed with dichloromethane to afford five subfractions SF1-SF5. Among the subfractions, SF5 was separated by silica gel column chromatography using dichloromethane and MeOH (10:1 to 1:1 gradient) to furnish lupenone (136.8 mg, 3.8%) and lupeol (28.8 mg, 0.8%). The isolated compounds were identified by comparison of their spectral data with literature values141516.

Bottom Line: Lupenone, lupeol, and taraxerol inhibited the gene expression and production of MUC5AC mucin induced by TNF-α from NCI-H292 cells, respectively.The 3 compounds inhibited the EGF or PMA-induced production of MUC5AC mucin in NCI-H292 cells.In addition, the results partly explain the mechanism of of Adenophora triphylla var. japonica as a traditional remedy for diverse inflammatory pulmonary diseases.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Chungnam National University School of Medicine, Daejeon, Korea.

ABSTRACT

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 α (TNF-α) 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-α 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.

No MeSH data available.


Related in: MedlinePlus