title: Salvianolic acid B inhibited PPARγ expression and attenuated weight gain in mice with high-fat diet-induced obesity.
abstract: OBJECTIVE
  Obesity contributes to the development of cardiometabolic disorders such as type 2 diabetes, fatty liver disease and cardiovascular disease. Salvianolic acid B (Sal B) is a molecule derived from the root of Salvia miltiorrhiza (Danshen), which is a traditional Chinese medicine that is widely used to treat cardiovascular diseases. However, the role of Sal B in obesity and obesity-related metabolic disorders is unknown. In this study, we aimed to investigate the effects of Sal B on high-fat diet-induced obesity and determine the possible mechanisms involved.
  
  
  METHODS
  Male C57BL/6J mice fed a high-fat diet for 12 weeks received a supplement of Sal B (100 mg/kg/day) by gavage for a further 8 weeks. These mice were compared to control mice fed an un-supplemented high-fat diet. 3T3-L1 preadipocytes were used in vitro studies.
  
  
  RESULTS
  Sal B administration significantly decreased body weight, white adipose tissue weight, adipocyte size and lipid (triglyceride and total cholesterol) levels in obese mice. Eight weeks of Sal B administration also improved the intraperitoneal glucose tolerance test (IPGTT) and intraperitoneal insulin tolerance test (IPITT) scores in high-fat diet-induced obese mice. In 3T3-L1 preadipocytes that were cultured in vitro and induced to differentiate, Sal B reduced the accumulation of lipid droplets and lipid content in a dose-dependent manner. Immunoblotting indicated that Sal B decreased peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα) expression but increased the expression of GATA binding protein 2 and 3 (GATA 2, GATA 3) both in vivo and in vitro.
  
  
  CONCLUSIONS
  Our data suggest that Sal B may reduce obesity and obesity-related metabolic disorders by suppressing adipogenesis. The effects of Sal B in adipose tissue may be related to its action on PPARγ, C/EBPα, GATA-2 and GATA-3.
authors.affiliation: Department of Cardiology, The First Affiliated Hospital, Chengdu Medical College, Chengdu, China.
authors.forename: Peijian
authors.initials: P
authors.lastname: Wang
authors.forename: Shuyu
authors.initials: S
authors.lastname: Xu
authors.forename: Wenzhang
authors.initials: W
authors.lastname: Li
authors.forename: Fang
authors.initials: F
authors.lastname: Wang
authors.forename: Zhen
authors.initials: Z
authors.lastname: Yang
authors.forename: Licheng
authors.initials: L
authors.lastname: Jiang
authors.forename: Qiulin
authors.initials: Q
authors.lastname: Wang
authors.forename: Mingqing
authors.initials: M
authors.lastname: Huang
authors.forename: Peng
authors.initials: P
authors.lastname: Zhou
mesh_terms: D041721:3T3-L1 Cells; D000818:Animals; D001572:Benzofurans / Q000494:pharmacology*; D059305:Diet, High-Fat; D006949:Hyperlipidemias / Q000517:prevention & control; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000209:etiology / Q000503:physiopathology*; D047495:PPAR gamma / Q000378:metabolism*; D015430:Weight Gain / Q000187:drug effects*; D053630:Depsides
chemical_list: D001572:Benzofurans; D047495:PPAR gamma; C076944:salvianolic acid B; D053630:Depsides