title: Hepatic stimulator substance alleviates toxin-induced and immune-mediated liver injury and fibrosis in rats.
abstract: BACKGROUND
  Liver fibrosis is a common scarring response to chronic liver injury. It is a precursor to cirrhosis and liver carcinoma. Hepatic stimulator substance (HSS), a known liver-specific but species-nonspecific growth factor, has been shown to protect hepatocytes from various toxins.
  
  
  METHODS
  We have investigated the effects of HSS therapy on carbon tetrachloride (CCl(4))-induced and porcine-serum-mediated hepatic injury and fibrosis. We hypothesize that HSS might attenuate liver injury and fibrosis by suppressing oxidative stress, down-regulating profibrogenic factors, and blocking HSCs activation.
  
  
  RESULTS
  This report demonstrated that HSS therapy diminished α-smooth muscle actin expression, decreased intrahepatic reactive oxygen species (ROS) level, and down-regulated transforming growth factor (TGF)-β1, platelet-derived growth factor (PDGF)-BB, and tissue inhibitor of metalloproteinase (TIMP)-1 expression. In addition, HSS treatment significantly protected the liver from injury by improving liver function tests and histological architecture of the liver.
  
  
  CONCLUSIONS
  These results provided novel insights into the mechanisms of HSS in the protection of the liver. Our results suggested that HSS might be a therapeutic antifibrotic agent for the treatment of liver fibrosis.
authors.affiliation: Key Laboratory of Liver Disease, Center of Infectious Diseases, Guangzhou 458 Hospital, Dongfengdonglu 801#, Guangzhou 510600, Guangdong, China.
authors.forename: Xuerui
authors.initials: X
authors.lastname: Yi
authors.forename: Ming
authors.initials: M
authors.lastname: Song
authors.forename: Youcheng
authors.initials: Y
authors.lastname: Yuan
authors.forename: Xinrui
authors.initials: X
authors.lastname: Zhang
authors.forename: Wenyin
authors.initials: W
authors.lastname: Chen
authors.forename: Jin
authors.initials: J
authors.lastname: Li
authors.forename: Minghua
authors.initials: M
authors.lastname: Tong
authors.forename: Guangze
authors.initials: G
authors.lastname: Liu
authors.forename: Song
authors.initials: S
authors.lastname: You
authors.forename: Xiangping
authors.initials: X
authors.lastname: Kong
mesh_terms: D000818:Animals; D000077214:Becaplermin; D002252:Carbon Tetrachloride Poisoning / Q000188:drug therapy*; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy*; D055166:Hepatic Stellate Cells / Q000187:drug effects; D036341:Intercellular Signaling Peptides and Proteins; D008099:Liver / Q000378:metabolism; D008103:Liver Cirrhosis / Q000188:drug therapy* / Q000378:metabolism; D008111:Liver Function Tests; D008297:Male; D008934:Mitogens / Q000494:pharmacology / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000187:drug effects; D010455:Peptides / Q000494:pharmacology / Q000627:therapeutic use*; D020574:Proto-Oncogene Proteins c-sis / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D013552:Swine; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D036341:Intercellular Signaling Peptides and Proteins; D008934:Mitogens; D010455:Peptides; D020574:Proto-Oncogene Proteins c-sis; D017382:Reactive Oxygen Species; D019715:Tissue Inhibitor of Metalloproteinase-1; D053773:Transforming Growth Factor beta1; C073456:hepatic stimulator substance; D000077214:Becaplermin