Open AccessEffects of astragaloside IV on pathogenesis of metabolic syndrome in vitro 1
Author(s) -
XU Mingen,
XIAO Shangzhi,
SUN Yonghong,
OUYANG Yang,
ZHENG Xiaoxiang
Publication year - 2006
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2006.00243.x
Subject(s) - adipogenesis , pathogenesis , intracellular , tumor necrosis factor alpha , flow cytometry , astragaloside , viability assay , apoptosis , peroxisome proliferator activated receptor , metabolic syndrome , chemistry , receptor , pharmacology , medicine , endocrinology , biology , biochemistry , microbiology and biotechnology , diabetes mellitus , in vitro , high performance liquid chromatography , chromatography
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.