title: Hyperbaric oxygen preconditioning induces tolerance against brain ischemia-reperfusion injury by upregulation of antioxidant enzymes in rats.
abstract: The present study examined the hypothesis that cerebral ischemic tolerance induced by hyperbaric oxygen preconditioning (HBO-PC) is associated with an increase of antioxidant enzyme activity. Male Sprague-Dawley rats (250-280 g, n=74) were divided into sham, middle cerebral artery occlusion (MCAO) for 90 min, and MCAO plus HBO-PC groups. HBO-PC was conducted four times by given 100% oxygen at 2.5 atmosphere absolute (ATA), for 1 h at every 12 h interval for 2 days. At 24 h after the last HBO-PC, MCAO was performed and at 24 h after MCAO, neurological function and Nissl Staining were performed to evaluate the effect of HBO-PC. Malondialdehyde (MDA) content, activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) sampled from the hippocampus, ischemic penumbra or core of cortex were measured. HBO-PC decreased mortality rate, improved neurological recovery, lessened neuronal injury, reduced the level of MDA and increased the antioxidant activity of CAT and SOD. These observations demonstrated that an upregulation of the antioxidant enzyme activity by HBO preconditioning plays an important role in the generation of tolerance against brain ischemia-reperfusion injury.
authors.affiliation: Department of Neurology, Changhai Hospital,174 Changhai Road, Shanghai 200433, PR China.
authors.forename: Jiasi
authors.initials: J
authors.lastname: Li
authors.forename: Wenwu
authors.initials: W
authors.lastname: Liu
authors.forename: Suju
authors.initials: S
authors.lastname: Ding
authors.forename: Weigang
authors.initials: W
authors.lastname: Xu
authors.forename: Yangtai
authors.initials: Y
authors.lastname: Guan
authors.forename: John H
authors.initials: JH
authors.lastname: Zhang
authors.forename: Xuejun
authors.initials: X
authors.lastname: Sun
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001921:Brain / Q000201:enzymology; D002545:Brain Ischemia / Q000201:enzymology* / Q000628:therapy; D002374:Catalase / Q000378:metabolism; D004789:Enzyme Activation; D004798:Enzymes / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006931:Hyperbaric Oxygenation; D020244:Infarction, Middle Cerebral Artery / Q000201:enzymology / Q000628:therapy; D019194:Ischemic Preconditioning; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D010101:Oxygen Consumption / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000201:enzymology* / Q000628:therapy; D013482:Superoxide Dismutase / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D015854:Up-Regulation
chemical_list: D000975:Antioxidants; D004798:Enzymes; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D002374:Catalase; C000606292:Sod1 protein, rat; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D005978:Glutathione; D010100:Oxygen