Effects of astragaloside IV on pathogenesis of metabolic syndrome in vitro1

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- 3 H]-deoxyglucose into the cells. The concentrations of peroxisome proliferator-activated receptor-γ (PPARγ) 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 Ca 2+ 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 μg/mL, improve high glucose-induced insulin resistance in adipocytes at a concentration of 30 μg/mL, and prevent tumor necrosis factor (TNF)-α-induced apoptosis and viability loss at concentrations of 10 and 30 μg/mL, and 30 μg/mL, respectively, in endothelial cells. Furthermore, we found that these effects were partly due to the promotion of PPARγ expression and to the inhibition of abnormal TNF-α-induced intracellular free Ca 2+ 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.