title: Baicalin Attenuates Cardiac Dysfunction and Myocardial Remodeling in a Chronic Pressure-Overload Mice Model.
abstract: OBJECTIVE
  Baicalin has been shown to be effective for various animal models of cardiovascular diseases, such as pulmonary hypertension, atherosclerosis and myocardial ischaemic injury. However, whether baicalin plays a role in cardiac hypertrophy remains unknown. Here we investigated the protective effects of baicalin on cardiac hypertrophy induced by pressure overload and explored the potential mechanisms involved.
  
  
  METHODS
  C57BL/6J-mice were treated with baicalin or vehicle following transverse aortic constriction or Sham surgery for up to 8 weeks, and at different time points, cardiac function and heart size measurement and histological and biochemical examination were performed.
  
  
  RESULTS
  Mice under pressure overload exhibited cardiac dysfunction, high mortality, myocardial hypertrophy, increased apoptosis and fibrosis markers, and suppressed cardiac expression of PPARα and PPARβ/δ. However, oral administration of baicalin improved cardiac dysfunction, decreased mortality, and attenuated histological and biochemical changes described above. These protective effects of baicalin were associated with reduced heart and cardiomyocyte size, lower fetal genes expression, attenuated cardiac fibrosis, lower expression of profibrotic markers, and decreased apoptosis signals in heart tissue. Moreover, we found that baicalin induced PPARα and PPARβ/δ expression in vivo and in vitro. Subsequent experiments demonstrated that long-term baicalin treatment presented no obvious cardiac lipotoxicity.
  
  
  CONCLUSIONS
  The present results demonstrated that baicalin attenuates pressure overload induced cardiac dysfunction and ventricular remodeling, which would be due to suppressed cardiac hypertrophy, fibrosis, apoptosis and metabolic abnormality.
authors.forename: Yanqing
authors.initials: Y
authors.lastname: Zhang
authors.forename: Pingping
authors.initials: P
authors.lastname: Liao
authors.forename: Meng'en
authors.initials: M
authors.lastname: Zhu
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Dan
authors.initials: D
authors.lastname: Hu
authors.forename: Siming
authors.initials: S
authors.lastname: Guan
authors.forename: Long
authors.initials: L
authors.lastname: Chen
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D002460:Cell Line; D048429:Cell Size; D004195:Disease Models, Animal; D004719:Endomyocardial Fibrosis / Q000209:etiology / Q000401:mortality / Q000473:pathology / Q000517:prevention & control*; D005419:Flavonoids / Q000494:pharmacology*; D005786:Gene Expression Regulation; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000401:mortality / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D047493:PPAR alpha / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D047494:PPAR delta / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D048068:PPAR-beta / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D011312:Pressure / Q000009:adverse effects; D015398:Signal Transduction; D016019:Survival Analysis; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000401:mortality / Q000473:pathology / Q000517:prevention & control*
chemical_list: D002316:Cardiotonic Agents; D005419:Flavonoids; D047493:PPAR alpha; D047494:PPAR delta; D048068:PPAR-beta; C038044:baicalin
keywords: Baicalin; Hypertrophy; Pressure overload