Effect of hyperbaric oxygen on apoptosis in neonatal hypoxia-ischemia rat model

John W. Calvert, Changman Zhou, Anil Nanda, John H. Zhang

Research output: Contribution to journalArticlepeer-review

82 Scopus citations

Abstract

We have previously demonstrated that a transient exposure to hyperbaric oxygen (HBO) attenuated the neuronal injury after neonatal hypoxia-ischemia. This study was undertaken to determine whether HBO offers this neuroprotection by reducing apoptosis in injured brain tissue. Seven-day-old rat pups were subjected to unilateral carotid artery ligation followed by 2 h of hypoxia (8% oxygen). Apoptotic cell death was examined in the injured cortex and hippocampus tissue. Caspase-3 expression and activity increased at 18 and 24 h after the hypoxia-ischemia insult. At 18-48 h, poly(ADP-ribose) polymerase (PARP) cleavage occurred, which reduced the band at 116 kDa and enhanced the band at 85 kDa. There was a time-dependent increase in the number of terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL)-positive cells. A single HBO treatment (100% oxygen, 3 ATA for 1 h) 1 h after hypoxia reduced the enhanced caspase-3 expression and activity, attenuated the PARP cleavage, and decreased the number of TUNEL-positive cells observed in the cortex and hippocampus. These results suggest that the neuroprotective effect of HBO is at least partially mediated by the reduction of apoptosis.

Original languageEnglish (US)
Pages (from-to)2072-2080
Number of pages9
JournalJournal of applied physiology
Volume95
Issue number5
DOIs
StatePublished - Nov 2003
Externally publishedYes

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Keywords

  • Caspase and caspase substrates
  • Neurodegeneration
  • Therapeutic effect

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