title: Effects of astragaloside IV on pathogenesis of metabolic syndrome in vitro.
abstract: OBJECTIVE
  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-gamma (PPARgamma) 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 microg/mL, improve high glucose-induced insulin resistance in adipocytes at a concentration of 30 microg/mL, and prevent tumor necrosis factor (TNF)-alpha-induced apoptosis and viability loss at concentrations of 10 and 30 microg/mL, and 30 microg/mL, respectively, in endothelial cells. Furthermore, we found that these effects were partly due to the promotion of PPARgamma expression and to the inhibition of abnormal TNF-alpha-induced intracellular free Ca(2+) accumulation in endothelial cells.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Biomedical Engineering, Hangzhou Dianzi University,Hangzhou 310018, China. xumingen@hziee.edu.cn
authors.forename: Ming-en
authors.initials: ME
authors.lastname: Xu
authors.forename: Shang-zhi
authors.initials: SZ
authors.lastname: Xiao
authors.forename: Yong-hong
authors.initials: YH
authors.lastname: Sun
authors.forename: Yang
authors.initials: Y
authors.lastname: Ou-Yang
authors.forename: Xiao-xiang
authors.initials: XX
authors.lastname: Zheng
mesh_terms: D017667:Adipocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D027885:Astragalus propinquus / Q000737:chemistry; D002118:Calcium / Q000378:metabolism*; D002454:Cell Differentiation / Q000187:drug effects; D002470:Cell Survival; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology*; D047495:PPAR gamma / Q000096:biosynthesis* / Q000235:genetics; D018517:Plant Roots / Q000737:chemistry; D010946:Plants, Medicinal / Q000737:chemistry; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D012503:Saponins / Q000302:isolation & purification / Q000494:pharmacology*; D014315:Triterpenes / Q000302:isolation & purification / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D047495:PPAR gamma; D012333:RNA, Messenger; D012503:Saponins; D014315:Triterpenes; D014409:Tumor Necrosis Factor-alpha; C052064:astragaloside A; D005947:Glucose; D002118:Calcium