title: Protective effects of baicalin on carbon tetrachloride induced liver injury by activating PPARγ and inhibiting TGFβ1.
abstract: BACKGROUND
  Traditional Chinese herbal medicines have attracted considerable attention in many countries with treatment of several end-stage liver diseases.
  
  
  OBJECTIVE
  The present study investigated the protective effects of baicalin on hepatotoxicity and hepatic fibrosis and explored the role of transforming growth factor β1 (TGFβ1) and peroxisome proliferator activated receptors γ (PPARγ) on the rat liver injury model.
  
  
  METHODS
  The rat liver injury model was introduced by subcutaneous injection of carbon tetrachloride (CCl(4)) for 8 weeks. At week 5, rats were treated with baicalin of different doses or silymarin. Detection of biochemical indicators, histological analysis, and enzyme-linked immunosorbent assays were employed to evaluate severity of liver inflammation, and western blotting and RT-PCR assay were performed to evaluate TGFβ1 and PPARγ pathway related proteins and gene expression.
  
  
  RESULTS
  The administration of baicalin could significantly improve histological changes of CCl(4) treated rat livers and return biochemical indicators for liver injury to nearly baseline level. In addition, the increased expression of TGFβ1 was markedly suppressed by baicalin, and decreased expression of PPARγ was also dramatically elevated by baicalin as well. The hepatoprotective effects of baicalin may be conferred by elevating the level of PPARγ contributing to down-regulation of TGFβ1 signaling pathway and suppression of hepatic stellate cell activation.
  
  
  CONCLUSIONS
  The studies demonstrated that baicalin is a potent and promising antifibrotic drug in the treatment of hepatic fibrosis.
authors.affiliation: College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
authors.forename: Hongxiang
authors.initials: H
authors.lastname: Qiao
authors.forename: Hongcan
authors.initials: H
authors.lastname: Han
authors.forename: Dongsheng
authors.initials: D
authors.lastname: Hong
authors.forename: Zihua
authors.initials: Z
authors.lastname: Ren
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Changxin
authors.initials: C
authors.lastname: Zhou
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002251:Carbon Tetrachloride / Q000633:toxicity; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005419:Flavonoids / Q000008:administration & dosage / Q000627:therapeutic use*; D005786:Gene Expression Regulation / Q000187:drug effects; D008103:Liver Cirrhosis / Q000188:drug therapy* / Q000503:physiopathology; D008107:Liver Diseases / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008516:Medicine, Chinese Traditional; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012720:Severity of Illness Index; D012838:Silymarin / Q000494:pharmacology; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D005419:Flavonoids; D047495:PPAR gamma; D012838:Silymarin; D053773:Transforming Growth Factor beta1; C038044:baicalin; D002251:Carbon Tetrachloride