Hydrogen therapy reduces apoptosis in neonatal hypoxia-ischemia rat model

Neurosci Lett. 2008 Aug 22;441(2):167-72. doi: 10.1016/j.neulet.2008.05.077. Epub 2008 May 24.

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.

MeSH terms

  • Animals
  • Animals, Newborn
  • Apoptosis / drug effects*
  • Caspase 12 / metabolism
  • Caspase 3 / metabolism
  • Cell Count / methods
  • Cerebral Cortex / pathology
  • Disease Models, Animal
  • Hippocampus / pathology
  • Hydrogen / therapeutic use*
  • Hypoxia-Ischemia, Brain / drug therapy*
  • Hypoxia-Ischemia, Brain / pathology
  • Hypoxia-Ischemia, Brain / physiopathology*
  • In Situ Nick-End Labeling / methods
  • Ligation / methods
  • Neurons / drug effects
  • Rats
  • Rats, Sprague-Dawley
  • Tetrazolium Salts
  • Time Factors

Substances

  • Tetrazolium Salts
  • triphenyltetrazolium
  • Hydrogen
  • Caspase 12
  • Caspase 3