Volume 16, Issue 1 (Spring 2012)                   Physiol Pharmacol 2012, 16(1): 54-61 | Back to browse issues page

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Alavian F, Hajizadeh S, Bigdeli M R, Bayat G R, Javan M. Evaluation of UCP2 expression in the phenomenon of ischemic resistance induced by alternating normobaric hyperoxia in a rat model of stroke. Physiol Pharmacol. 2012; 16 (1) :54-61
URL: http://ppj.phypha.ir/article-1-768-en.html
Abstract:   (11319 Views)
Introduction: ischemic preconditioning is one of the most important mechanisms, responsible for the increased brain resistance after stroke. One of the most important candidates to ischemia preconditioning is intermittent normobaric hyperoxia. In this study, the effect of intermittent normobaric hyperoxia on the expression of UCP2 was investigated in a stroke model. Methods: Rats were divided into 4 groups (normoxia – sham, hyperoxia – sham, normoxia – stroke and hyperoxia – stroke). Hyperoxia groups were exposed to 95% inspired O2, for 4 h/day and 6 consecutive days. Oxygen level in the control groups was %21 (normoxia). After 24 h, stroke groups were subjected to 60 min of right middle cerebral artery occlusion. After 24 h reperfusion neurological deficit scores were assessed. The brain UCP2 levels were analyzed by western blot. Results: The results of this study showed that following brain ischemia-reperfusion, UCP2 levels significantly increased in the stroke groups compared with the sham group while there was no significant difference in hyperoxia groups compared with normoxia. Also hyperoxia decreased neurological deficit scores. Conclusion: Following ischemia, oxidative stress caused by increase of ROS, leads to increased UCP2 levels in stroke groups. In this study, the neuroprotective effect of hyperoxia is independent of UCP2 expression.
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