Robert P. Ostrowski,1 Gerhart Graupner,2 Elena Titova,1 Jennifer Zhang,1 Jeffrey Chiu,1 Neal Dach,1 Dalia Corleone,1 Jiping Tang,1 and John H. Zhang1,3,4, Neurobiol Dis. 2008 January; 29(1): 1–13.
1 Department of Physiology and Pharmacology, Loma Linda University, USA
2 Department of Pediatrics, Loma Linda University, USA
3 Department of Neurosurgery, Loma Linda University, USA
4 Department of Anesthesiology, Loma Linda University, USA
Correspondence to: Dr John H. Zhang, Department of Physiology & Pharmacology, Risley Hall, Room 219, Loma Linda University School of Medicine, Loma Linda, CA 92350, Tel: (909) 558–4723; Fax: (909) 558–0119, E-mail: johnzhang3910@yahoo.com
Abstract
We hypothesized that the brain-protective effect of hyperbaric oxygen (HBO) preconditioning in a transient global cerebral ischemia rat model is mediated by the inhibition of early apoptosis.
One hundred ten male Sprague Dawley (SD) rats (300–350 g body weight) were allocated to the sham group and three other groups with 10 minutes of four-vessel occlusion, untreated or preconditioned with either 3 or 5 hyperbaric oxygenations. HBO preconditioning improved neurobehavioral scores and reduced mortality, decreased ischemic cell change, reduced the number of early apoptotic cells and hampered a conversion of early to late apoptotic alterations. HBO preconditioning reduced the immunoreactivity of phosphorylated p38 in vulnerable neurons and increased the expression of brain derived neurotrophic factor (BDNF) in early stage post-ischemia. However, preconditioning with 3 HBO treatments proved less beneficial than with 5 HBO treatments.
We conclude that HBO preconditioning may be neuroprotective by reducing early apoptosis and inhibition of the conversion of early to late apoptosis, possibly through an increase in brain BDNF level and the suppression of p38 activation.
Keywords: Hyperbaric oxygen preconditioning, Annexin V, Apoptosis, Global cerebral ischemia, BDNF, p38 | 
