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1.
Tuberculosis and Respiratory Diseases ; : 210-217, 2015.
Article in English | WPRIM | ID: wpr-114247

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 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.


Subject(s)
Campanulaceae , Enzyme-Linked Immunosorbent Assay , Epidermal Growth Factor , Epithelial Cells , Gene Expression , Lung Diseases , Medicine, Traditional , Methods , Mucins , Tumor Necrosis Factor-alpha
2.
Chinese Journal of Natural Medicines (English Ed.) ; (6): 391-395, 2013.
Article in English | WPRIM | ID: wpr-812664

ABSTRACT

AIM@#To study the chemical constituents and their anti-amnesic effect from the hooks of Uncaria rhynchophylla.@*METHODS@#The isolation of compounds was performed by chromatographic techniques and their structures were identified on the basis of spectral analysis. Their ameliorating effects on scopolamine-induced memory impairment in vivo using a Morris water-maze task and passive avoidance task system were evaluated.@*RESULTS@#Activity-guided fractionation of the total extracts resulted in the isolation of four constituents, trans-anethole (1), p-anisaldehyde (2), estragole (3), and 3-oxo-olean-12-en-28-oic acid (4), which were found for the first time from this plant.@*CONCLUSION@#Compound 1 exhibited a better memory enhancing effect than tacrine, a positive agent, at the same dose in the passive avoidance test and a similar property in the water-maze test, and its action may be mediated, in part, by the acetylcholine enhancing cholinergic nervous system.


Subject(s)
Animals , Humans , Male , Rats , Memory , Memory Disorders , Drug Therapy , Molecular Structure , Plant Extracts , Chemistry , Rats, Sprague-Dawley , Scopolamine , Uncaria , Chemistry
3.
The Korean Journal of Physiology and Pharmacology ; : 157-162, 2011.
Article in English | WPRIM | ID: wpr-727887

ABSTRACT

Vascular inflammation process has been suggested to be an important risk factor in the development of atherosclerosis. Recently we reported that induction of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) selectively inhibits vascular cell adhesion molecule-1 (VCAM-1) but not intercellular cell adhesion molecule-1 (ICAM-1) in tumor necrosis factor (TNF)-alpha-activated human umbilical vein endothelial cells (HUVEC). In this study, we investigated whether genipin inhibits expression of cellular adhesion molecules, which is relevant to inflammation. Pretreatment with genipin reduced reactive oxygen species (ROS) production and expression of VCAM-1, but not ICAM-1 in TNF-alpha-activated HUVEC. Genipin dose- and time-dependently increased PPAR-gamma expression and inhibited TNF-alpha-induced phosphorylation of Akt and PKC with different degrees. Finally, genipin prevented TNF-alpha-induced adhesion of U937 monocytic cells to HUVEC. Taken together, these results indicate that upregualtion of PPAR-gamma by genipin selectively inhibits TNF-alpha-induced expression of VCAM-1, in which regulation of Akt and/or PKC play a key role. We concluded that genipin can be used for the treatment of cardiovascular disorders such as atherosclerosis.


Subject(s)
Humans , Atherosclerosis , Cell Adhesion , Endothelial Cells , Human Umbilical Vein Endothelial Cells , Inflammation , Intercellular Adhesion Molecule-1 , Iridoids , Peroxisomes , Phosphorylation , Reactive Oxygen Species , Risk Factors , Tumor Necrosis Factor-alpha , Up-Regulation , Vascular Cell Adhesion Molecule-1
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