TY - JOUR
T1 - Hydrogen therapy reduces apoptosis in neonatal hypoxia-ischemia rat model
AU - Cai, Jianmei
AU - Kang, Zhimin
AU - Liu, Wen Wu
AU - Luo, Xu
AU - Qiang, Sun
AU - Zhang, John H.
AU - Ohta, Shigeo
AU - Sun, Xuejun
AU - Xu, Weigang
AU - Tao, Hengyi
AU - Li, Runping
N1 - 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 °C).
PY - 2008/8/22
Y1 - 2008/8/22
N2 - 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 °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. © 2008 Elsevier Ireland Ltd. All rights reserved.
AB - 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 °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. © 2008 Elsevier Ireland Ltd. All rights reserved.
KW - Apoptosis
KW - Hydrogen
KW - Hydroxyl radical
KW - Hypoxic ischemia
KW - Animals, Newborn
KW - Hippocampus/pathology
KW - Caspase 3/metabolism
KW - In Situ Nick-End Labeling/methods
KW - Cerebral Cortex/pathology
KW - Apoptosis/drug effects
KW - Rats
KW - Neurons/drug effects
KW - Ligation/methods
KW - Cell Count/methods
KW - Rats, Sprague-Dawley
KW - Hypoxia-Ischemia, Brain/drug therapy
KW - Tetrazolium Salts
KW - Animals
KW - Caspase 12/metabolism
KW - Time Factors
KW - Hydrogen/therapeutic use
KW - Disease Models, Animal
UR - http://www.scopus.com/inward/record.url?scp=46749107977&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=46749107977&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/8ccd5c25-ab17-3bd9-96c3-e9f714c1e3d6/
U2 - 10.1016/j.neulet.2008.05.077
DO - 10.1016/j.neulet.2008.05.077
M3 - Article
C2 - 18603371
SN - 0304-3940
VL - 441
SP - 167
EP - 172
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 2
ER -