title: Hydrogen therapy reduces apoptosis in neonatal hypoxia-ischemia rat model.
abstract: Hypoxia-ischemia (HI) brain injury is a major cause of neuronal cell death especially apoptosis in the perinatal period. This study was designated to examine the effect of hydrogen therapy on apoptosis in an established neonatal HI rat pup model. Seven-day-old rat pups were subjected to left common carotid artery ligation and then 90 min hypoxia (8% oxygen at 37 degrees C). Immediately after HI insult, pups were placed into a chamber filled with 2% H2 for 30 min, 60 min, or 120 min, respectively. 24 h after 2% H2 therapy, the pups were decapitated and brain injury was assessed by 2,3,5-triphenyltetrazoliumchloride (TTC), Nissl, and TUNEL staining, as well as caspase-3, caspase-12 activities in the cortex and hippocampus. H2 treatment in a duration-dependent manner significantly reduced the number of positive TUNEL cells and suppressed caspase-3 and -12 activities. These results indicated H2 administration after HI appeared to provide brain protection via inhibition of neuronal apoptosis.
authors.affiliation: Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433, PR China.
authors.forename: Jianmei
authors.initials: J
authors.lastname: Cai
authors.forename: Zhimin
authors.initials: Z
authors.lastname: Kang
authors.forename: Wen Wu
authors.initials: WW
authors.lastname: Liu
authors.forename: Xu
authors.initials: X
authors.lastname: Luo
authors.forename: Sun
authors.initials: S
authors.lastname: Qiang
authors.forename: John H
authors.initials: JH
authors.lastname: Zhang
authors.forename: Shigeo
authors.initials: S
authors.lastname: Ohta
authors.forename: Xuejun
authors.initials: X
authors.lastname: Sun
authors.forename: Weigang
authors.initials: W
authors.lastname: Xu
authors.forename: Hengyi
authors.initials: H
authors.lastname: Tao
authors.forename: Runping
authors.initials: R
authors.lastname: Li
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects*; D053454:Caspase 12 / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D002452:Cell Count / Q000379:methods; D002540:Cerebral Cortex / Q000473:pathology; D004195:Disease Models, Animal; D006624:Hippocampus / Q000473:pathology; D006859:Hydrogen / Q000627:therapeutic use*; D020925:Hypoxia-Ischemia, Brain / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D020287:In Situ Nick-End Labeling / Q000379:methods; D008026:Ligation / Q000379:methods; D009474:Neurons / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013778:Tetrazolium Salts; D013997:Time Factors
chemical_list: D013778:Tetrazolium Salts; C009591:triphenyltetrazolium; D006859:Hydrogen; D053454:Caspase 12; D053148:Caspase 3