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Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue.
Brain Res. 2009 Mar 13; 1260:47-54.BR

Abstract

Recent studies suggest that normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced upregulation of antioxidant enzymes. Rodents comprised five groups, breathing room air (RA; O(2)=21%), or 95% oxygen (hyperoxia, HO) for 4, 8, 16, and 24 h (RA, 4HO, 8HO, 16HO, 24HO respectively) in the same chamber. Each main group was subdivided to MCAO-operated (middle cerebral artery occlusion), and intact (without any surgery) subgroups. After 24 h, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS), mortality rate, and infarct volume were measured in MCAO-operated subgroups. 48 h after pretreatment, antioxidant enzymes activities were assessed in MCAO-operated, sham-operated, and intact subgroups. Preconditioning with 16HO and 24HO decreased NDS, mortality rate, infarct volume, and increased antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, the prolonged HO seems to partly exert their effects via increase in antioxidant enzymes activities.

Authors+Show Affiliations

Faculty of Biological Sciences, Shahid Beheshti University, G.C., Tehran, Iran. bigdelimohammadreza@yahoo.com

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19167368

Citation

Bigdeli, Mohammad Reza. "Preconditioning With Prolonged Normobaric Hyperoxia Induces Ischemic Tolerance Partly By Upregulation of Antioxidant Enzymes in Rat Brain Tissue." Brain Research, vol. 1260, 2009, pp. 47-54.
Bigdeli MR. Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue. Brain Res. 2009;1260:47-54.
Bigdeli, M. R. (2009). Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue. Brain Research, 1260, 47-54. https://doi.org/10.1016/j.brainres.2008.12.065
Bigdeli MR. Preconditioning With Prolonged Normobaric Hyperoxia Induces Ischemic Tolerance Partly By Upregulation of Antioxidant Enzymes in Rat Brain Tissue. Brain Res. 2009 Mar 13;1260:47-54. PubMed PMID: 19167368.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue. A1 - Bigdeli,Mohammad Reza, Y1 - 2009/01/07/ PY - 2008/11/04/received PY - 2008/12/14/revised PY - 2008/12/17/accepted PY - 2009/1/27/entrez PY - 2009/1/27/pubmed PY - 2009/3/27/medline SP - 47 EP - 54 JF - Brain research JO - Brain Res. VL - 1260 N2 - Recent studies suggest that normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced upregulation of antioxidant enzymes. Rodents comprised five groups, breathing room air (RA; O(2)=21%), or 95% oxygen (hyperoxia, HO) for 4, 8, 16, and 24 h (RA, 4HO, 8HO, 16HO, 24HO respectively) in the same chamber. Each main group was subdivided to MCAO-operated (middle cerebral artery occlusion), and intact (without any surgery) subgroups. After 24 h, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS), mortality rate, and infarct volume were measured in MCAO-operated subgroups. 48 h after pretreatment, antioxidant enzymes activities were assessed in MCAO-operated, sham-operated, and intact subgroups. Preconditioning with 16HO and 24HO decreased NDS, mortality rate, infarct volume, and increased antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, the prolonged HO seems to partly exert their effects via increase in antioxidant enzymes activities. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/19167368/Preconditioning_with_prolonged_normobaric_hyperoxia_induces_ischemic_tolerance_partly_by_upregulation_of_antioxidant_enzymes_in_rat_brain_tissue_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(08)03097-7 DB - PRIME DP - Unbound Medicine ER -