title: Protective effects of hydrogen-rich saline in a rat model of traumatic brain injury via reducing oxidative stress.
abstract: BACKGROUND
  Hydrogen gas (H(2)) has been considered as a novel antioxidant to selectively reduce the toxic reactive oxygen species (ROS) such as hydroxyl radical (•OH) without affecting the other signal ROS. Our recent study shows that H(2) inhalation is beneficial to traumatic brain injury (TBI) via reducing oxidative stress. In contrast to H(2), hydrogen-rich saline (HS) may be more suitable for clinical application. The present study was designed to investigate whether HS has a protective effect against TBI via reducing oxidative stress in rats.
  
  
  METHODS
  TBI model was induced by controlled cortical impact injury. Different dosages of HS were intraperitoneally administered at 5 min after TBI operation. We then measured the brain edema, blood-brain barrier (BBB) breakdown, neurological dysfunction and injury volume in all animals. In addition, the oxidative products and antioxidant enzymes in brain tissues were detected.
  
  
  RESULTS
  TBI-challenged rats exhibited significant brain injuries characterized by the increase of BBB permeability, brain edema, and lesion volume as well as neurological dysfunction, which were dose-dependently ameliorated by HS treatment. Moreover, we found that HS treatment increased the endogenous antioxidant enzymatic activities and decreased the oxidative product levels in brain tissues of TBI-challenged rats.
  
  
  CONCLUSIONS
  Hydrogen-rich saline can exert a protective effect against TBI via reducing oxidative stress. Molecular hydrogen may be a more effective therapeutic strategy for TBI patients.
authors.affiliation: Department of Neurosurgery, Xijing Institute of Clinical Neuroscience, Xiing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, PR China.
authors.forename: Xituan
authors.initials: X
authors.lastname: Ji
authors.forename: Ye
authors.initials: Y
authors.lastname: Tian
authors.forename: Keliang
authors.initials: K
authors.lastname: Xie
authors.forename: Weiping
authors.initials: W
authors.lastname: Liu
authors.forename: Yan
authors.initials: Y
authors.lastname: Qu
authors.forename: Zhou
authors.initials: Z
authors.lastname: Fei
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D001812:Blood-Brain Barrier / Q000378:metabolism; D001929:Brain Edema / Q000188:drug therapy / Q000378:metabolism; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D006859:Hydrogen / Q000008:administration & dosage*; D007263:Infusions, Parenteral; D008297:Male; D009043:Motor Activity / Q000502:physiology; D018696:Neuroprotective Agents / Q000008:administration & dosage; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D020127:Recovery of Function / Q000502:physiology; D012965:Sodium Chloride / Q000008:administration & dosage*
chemical_list: D000975:Antioxidants; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D012965:Sodium Chloride; D006859:Hydrogen