Repository of Research and Investigative Information

Repository of Research and Investigative Information

Baqiyatallah University of Medical Sciences

In vivo preconditioning with normobaric hyperoxia induces ischemic tolerance partly by triggering tumor necrosis factor-α converting enzyme/tumor necrosis factor-α/nuclear factor-κB

(2008) In vivo preconditioning with normobaric hyperoxia induces ischemic tolerance partly by triggering tumor necrosis factor-α converting enzyme/tumor necrosis factor-α/nuclear factor-κB. Neuroscience. pp. 671-678. ISSN 03064522 (ISSN)

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Recent studies suggest that intermittent and prolonged normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced BIT, and to explore the putative roles of tumor necrosis factor-α (TNF-α) converting enzyme (TACE), TNF-α, and nuclear factor-κB (NF-κB) activation in mediating this effect. Two core experimental protocols were applied to rats (experiments 1 E1 and 2 E2 respectively). E1 rodents comprised six subgroups, breathing room air (RA; O2=21%), or 95% oxygen (HO) for 4, 8, 16 h (4RA, 8RA, 16RA and 4HO, 8HO, 16HO respectively). E2 rodents were divided into subgroups, exposed to 95% inspired HO for 4 h/day for six consecutive days (intermittent hyperoxia, InHO) or for 24 continuous hours (prolonged hyperoxia, PrHO). Each of these had a control group exposed to 21% oxygen in the same chamber. Twenty-four hours after pretreatment, each group was randomly divided to receive 60 min right middle cerebral artery occlusion (MCAO-operated), sham-operation (without MCAO), or no operation (intact). After 24 h reperfusion, neurologic deficit score (NDS), brain water content, Evans Blue extravasation (as a marker of blood-brain barrier permeability), TACE expression, serum TNF-α, and phosphor- κBα levels were assessed in all animals, and infarct volume in the MCAO-operated subgroups. E1: Compared with the control (RA) group, infarct volume was reduced by 58.6% and 64.4% in 16 h and 24 h respectively. NDS and Evans Blue extravasation was also reduced in 16 h and 24 h. There was no statistical difference among 4 h and 8 h. E2: Preconditioning with prolonged and intermittent HO decreased NDS, infarct volume and upregulated TACE and increased phosphor-κBα and serum TNF-α level significantly. Although further studies are needed to clarify the mechanisms of brain ischemic tolerance, InHO and PrHO may partly exert their effects via triggering TACE/TNF-α/NF-κB. © 2008 IBRO.

Item Type: Article
Keywords: ischemic preconditioning ischemic tolerance NF-κB normobaric hyperoxia TACE TNF-a Evans blue immunoglobulin enhancer binding protein oxygen tumor necrosis factor alpha tumor necrosis factor alpha converting enzyme ambient air animal experiment animal model animal tissue article blood brain barrier brain ischemia brain water conditioning control group controlled study extravasation hyperoxia in vivo study male membrane permeability middle cerebral artery occlusion nonhuman occlusive cerebrovascular disease oxygen tension priority journal protein blood level protein expression rat reperfusion scoring system sham procedure statistical significance ADAM Proteins Animals Blood-Brain Barrier Blotting, Western Enzyme-Linked Immunosorbent Assay Infarction, Middle Cerebral Artery NF-kappa B Rats Rats, Sprague-Dawley Tumor Necrosis Factor-alpha Up-Regulation
Page Range: pp. 671-678
Journal or Publication Title: Neuroscience
Journal Index: Scopus
Volume: 153
Number: 3
Identification Number:
ISSN: 03064522 (ISSN)
Depositing User: مهندس مهدی شریفی

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