EFFECTS OF PRECONDITIONING WITH NORMOBARIC HYPEROXIA ON NA+/CA2+ EXCHANGER IN THE RAT BRAIN

被引:14
|
作者
Mohammadi, E. [1 ]
Bigdeli, M. R. [1 ]
机构
[1] Shahid Beheshti Univ, Dept Physiol, Fac Biol Sci, Tehran, Iran
基金
美国国家科学基金会;
关键词
Na+-Ca2+ exchanger; normobaric hyperoxia; brain ischemia; reperfusion; stroke; neuroprotection; CEREBRAL-ARTERY OCCLUSION; C6; GLIOMA-CELLS; FACTOR-KAPPA-B; ISCHEMIC TOLERANCE; NA+/CA2+ EXCHANGER; NA+-CA2+ EXCHANGER; UP-REGULATION; GLUTAMATE TRANSPORTERS; CHEMICAL HYPOXIA; GENE-EXPRESSION;
D O I
10.1016/j.neuroscience.2013.01.064
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background Recent studies suggest that normobaric hyperoxia (HO) reduces hypoxia-reoxygenation injury in the rat brain. We have attempted to determine the effect of HO on Na+-Ca2+ exchangers (NCX) in the rat stroke model. Methods: Rats were divided into two experimental groups. The first group was exposed to 95% inspired HO for 4 h/day for 6 consecutive days (HO). The second group acted as the control, and was exposed to 21% oxygen in the same chamber. Each main group was subdivided to middle cerebral artery occlusion (MCAO-operated) and intact (without any surgery) subgroups. After 48 h from pretreatment, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS) and infarct volume were measured in MCAO-operated subgroups. The NCXs expression levels of the core, penumbra and subcortical regions were assessed in sham-operated and intact subgroups. Result: Preconditioning with HO decreased NDS and infarct volume, and increased the expression of NCX1, NCX2 and NCX3 in the penumbra, NCX2, NCX3 in the core and NCX1 and NCX3 in the subcortex. Conclusion: Although further studies are needed to clarify the mechanisms of ischemic tolerance, HO partly is associated with the expression of NCX1, 2, 3 consistent with an active role in the genesis of ischemic protection. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:277 / 284
页数:8
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