title: The protective role of hydrogen-rich saline in experimental liver injury in mice.
abstract: OBJECTIVE
  Reactive oxygen species (ROS) are considered to play a prominent causative role in the development of various hepatic disorders. Antioxidants have been effectively demonstrated to protect against hepatic damage. Hydrogen (H(2)), a new antioxidant, was reported to selectively reduce the strongest oxidants, such as hydroxyl radicals (·OH) and peroxynitrite (ONOO(-)), without disturbing metabolic oxidation-reduction reactions or disrupting ROS involved in cell signaling. In place of H(2) gas, hydrogen-rich saline (HS) may be more suitable for clinical application. We herein aim to verify its protective effects in experimental models of liver injury.
  
  
  METHODS
  H(2) concentration in vivo was detected by hydrogen microelectrode for the first time. Liver damage, ROS accumulation, cytokine levels, and apoptotic protein expression were, respectively, evaluated after GalN/LPS, CCl(4), and DEN challenge. Simultaneously, CCl(4)-induced hepatic cirrhosis and DEN-induced hepatocyte proliferation were measured.
  
  
  RESULTS
  HS significantly increased hydrogen concentration in liver and kidney tissues. As a result, acute liver injury, hepatic cirrhosis, and hepatocyte proliferation were reduced through the quenching of detrimental ROS. Activity of pro-apoptotic players, such as JNK and caspase-3, were also inhibited.
  
  
  CONCLUSIONS
  HS could protect against liver injury and also inhibit the processes leading to liver cirrhosis and hepatocyte compensatory proliferation.
authors.affiliation: International Co-operation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai 200438, PR China.
authors.forename: HanYong
authors.initials: H
authors.lastname: Sun
authors.forename: Lei
authors.initials: L
authors.lastname: Chen
authors.forename: WeiPing
authors.initials: W
authors.lastname: Zhou
authors.forename: Liang
authors.initials: L
authors.lastname: Hu
authors.forename: Liang
authors.initials: L
authors.lastname: Li
authors.forename: QianQian
authors.initials: Q
authors.lastname: Tu
authors.forename: YanXin
authors.initials: Y
authors.lastname: Chang
authors.forename: Qu
authors.initials: Q
authors.lastname: Liu
authors.forename: XueJun
authors.initials: X
authors.lastname: Sun
authors.forename: MengChao
authors.initials: M
authors.lastname: Wu
authors.forename: HongYang
authors.initials: H
authors.lastname: Wang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage* / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D056486:Chemical and Drug Induced Liver Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D006859:Hydrogen / Q000008:administration & dosage* / Q000378:metabolism; D007274:Injections, Intraperitoneal; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008106:Liver Cirrhosis, Experimental / Q000517:prevention & control; D017114:Liver Failure, Acute / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D012965:Sodium Chloride / Q000008:administration & dosage*
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D012965:Sodium Chloride; D006859:Hydrogen; D048031:JNK Mitogen-Activated Protein Kinases