Firoozeh Alavian, Sohrab Hajizadeh, Mohammad Javan, Roham Mazloom,
Volume 20, Issue 6 (9-2017)
Abstract
Background: Recent studies indicate that hyperoxia has a significant therapeutic effect in the acute ischemic injury. The role of intracellular kinases, including ERK, has been posed in the phenomenon of ischemic tolerance. In the present study, the effect of intermittent normobaric hyperoxia on the activity of ERK in the stroke model was studied
Material and Methods: This is an experimental study. Animals include 4 groups (sham, hyperoxia–sham, stroke and hyperoxia–stroke); each group consisted of 6 male Wistar rats in the weight range of 250 to 350 grams. Hyperoxia groups were exposed to 95% inspired oxygen for 4 h/day and 6 consecutive days. Oxygen concentration in the control groups was 21% (normoxia, room air). After 24h, the stroke group animals were subjected to 60 min of right middle cerebral artery occlusion (MCAO). After 24h reperfusion, neurological deficit scores (NDS) and ERK activity were assessed.
Results: 5 hours after MCAO, stroke groups showed a significant increase in ERK activity in the cortex (p <0.01) and subcortex (p <0.001). At the same time, hyperoxia significantly increased the activity of ERK in cortex compared to the normoxia group (p<0.05). In subcortex, hyperoxia had no significant effect on ERK activity. Twenty-four hours after MCAO, stroke groups showed a significant reduction in ERK activity in the cortex (p <0.001) and subcortex (p <0.05). 24hr after MCAO, The activity of ERK in the hyperoxia groups; in both cortex and subcortex areas was significantly higher than that of the normoxia groups (p<0.05). Also, hyperoxia caused a significant decrease in NDS (p=0.0220).
Conclusion: Increased levels of ERK activity in the hyperoxia groups can be used to protect the nervous system, but the presence of other malicious factors may have been more effective in some cases, so that hyperoxia alone hasn’t been able to prevent stroke progression.
