Effects of preconditioning with intermittent normobaric hyperoxia on TNFR1 and TNFR2 expression in the rat brain

Recent studies have shown that intermittent normobaric hyperoxia (HO) protects the rat brain from ischemia reperfusion injury. However, the exact mechanism of this kind of protection in vivo is not known. In this study, the effect of HO on expression of TNFR1 and TNFR2 in a stroke model was investigated.
In this experimental study, rats were divided into 4 groups: normoxia – sham, hyperoxia – sham, normoxia – stroke and hyperoxia –stroke for each factor (TNFR1 or TNFR2). 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 rats were subjected to 60 min of right middle cerebral artery occlusion (MCAO). After 24h reperfusion, neurological deficit scores (NDS) and TNFR1, 2 brain levels using Western Blot were assessed.
Preconditioning with HO decreased NDS. Also, followed by stroke and reperfusion, TNFR1 levels significantly increased; while there was no significant difference in hyperoxia groups compared with normoxia groups in the cortex, HO significantly reduced TNFR1 expression in subcortex. On the other hand, groups of stroke compared to sham groups significantly expressed lower levels of TNFR2 in the cortex and subcortex. There was no significant difference in hyperoxia groups compared with normoxia groups in these areas.
Although additional studies will be required to further elucidate precise mechanisms of ischemic tolerance, it seems that HO is associated with the expression of TNFR1 in subcortex, consistent with an active role in the genesis of ischemic protection.