期刊
ACTA PHARMACOLOGICA SINICA
卷 27, 期 2, 页码 229-236出版社
NATURE PUBLISHING GROUP
DOI: 10.1111/j.1745-7254.2006.00243.x
关键词
astragaloside IV; metabolic syndrome X; insulin resistance; peroxisome proliferator-activated receptors; apoptosis; calcium
Aim: To investigate the diverse pharmacological actions of astragaloside IV from the perspective of metabolic syndrome, and to investigate the effect of the drug on the pathogenesis of metabolic syndrome. Methods: Adipogenesis was used as an indicator of the effect of astragaloside IV on preadipocyte differentiation, and was measured by using an oil red O assay. Glucose uptake was determined by measuring the transport of [2-H-3]-deoxyglucose into the cells. The concentrations of peroxisome proliferator-activated receptor-gamma(PPAR gamma) and aP2 mRNA were determined by using reverse transcription-polymerase chain reaction. Apoptosis and viability loss of endothelial cells were detected by using flow cytometry and the WST-1 assay, respectively. Intracellular free Ca2+ was labeled with Fluo-3 AM and measured by using a laser scanning confocal microscope. Results: Astragaloside IV can significantly potentiate insulin-induced preadipocyte differentiation at concentrations of 3, 10, and 30 mu g/mL, improve high glucose-induced insulin resistance in adipocytes at a concentration of 30 mu g/mL, and prevent tumor necrosis factor (TNF)-alpha-induced apoptosis and viability loss at concentrations of 10 and 30 mu g/mL, and 30 mu g/mL, respectively, in endothelial cells. Furthermore, we found that these effects were partly due to the promotion of PPAR gamma expression and to the inhibition of abnormal TNF-alpha-induced intracellular free Ca2+ accumulation in endothelial cells. Conclusion: The diverse pharmacological actions of astragaloside IV can all be linked to metabolic syndrome pathogenesis. Our study provides a new insight into the mechanism by which astragaloside IV exerts its effect.
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