Hyperbaric oxygen preconditioning reduces ischemia-reperfusion injury by inhibition of apoptosis via mitochondrial pathway in rat brain.

Abstract

This study examined the hypothesis that apoptotic inhibition via mitochondrial pathway was involved in hyperbaric oxygen preconditioning (HBO-PC)-induced neuroprotection on ischemia-reperfusion injury in rat brain. Male Sprague-Dawley rats (250 approximately 280 g, n=144) were divided into control, middle cerebral artery occlusion (MCAO) for 90 min, and HBO-PC plus MCAO groups. HBO-PC was conducted four times by giving 100% oxygen at 2.5 atm absolute (ATA), for 1 h at 12 h intervals for 2 days. At 24 h after the last HBO-PC, MCAO was performed and at 24 h after MCAO, neurological function, brain water content, infarct volume, and cell death were evaluated. Enzymatic activity of capase-3 and -9, and expression of cytochrome c, Bcl-2 and Bax proteins were performed in the samples from hippocampus, ischemic penumbra and core of the brain cortex, respectively. HBO-PC reduced brain edema, decreased infarction volume, and improved neurological recovery. HBO-PC reduced cytoplasm cytochrome c levels, decreased caspase enzyme activity, upregulated the ratio of Bcl-2 and Bax expression, and abated the apoptosis of ischemic tissue. HBO-PC protects brain tissues from ischemia-reperfusion injury by suppressing mitochondrial apoptotic pathways.

• Authors: J-S Li, W Zhang, Z-M Kang, S-J Ding, W-W Liu, J H Zhang, Y-T Guan, X-J Sun
• Journal: Neuroscience (Neuroscience) Vol. 159 Issue 4 Pg. 1309-15 (Apr 10 2009) ISSN: 1873-7544 [Electronic] United States
• PMID: 19185051 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Bax protein, rat
• Proto-Oncogene Proteins c-bcl-2
• bcl-2-Associated X Protein
• Water
• Cytochromes c
• Casp3 protein, rat
• Casp9 protein, rat
• Caspase 3
• Caspase 9

Topics

• Animals
• Apoptosis (physiology)
• Brain (pathology, physiopathology)
• Caspase 3 (metabolism)
• Caspase 9 (metabolism)
• Cerebral Cortex (pathology, physiopathology)
• Cytochromes c (metabolism)
• Hippocampus (pathology, physiopathology)
• Hyperbaric Oxygenation
• Infarction, Middle Cerebral Artery (pathology, physiopathology)
• Male
• Mitochondria (physiology)
• Motor Activity (physiology)
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• Random Allocation
• Rats
• Rats, Sprague-Dawley
• Reperfusion Injury (pathology, prevention & control, therapy)
• Water (metabolism)
• bcl-2-Associated X Protein (metabolism)