Effect Of Hyperbaric Oxygen On The Expression Of Survivin In Rat Brain Tissue After Severe Traumatic Brain Injury

Objective:Cumulative evidence suggests that apoptosis occurs after traumatic brain injury (TBI) from experimental models to humans. Recent experimental data have shown that the neuronprotective effect of hyperbaric oxygen therapy (HBOT) may represent the consequence of reduction of the mitochondrial pathway of apoptosis. Survivin attenuates apoptosis by inhibiting caspase-3. Some data demonstrate that survivin is abundantly expressed in both astrocytes and a subset of neurons of adult rats subjected to TBI.And another data suggests that strong up-regulation of survivin in brain tissue after TBI in rats may attenuate DNA cleavage and cell death. There have been no studies to demonstrate the relationship between the effect of HBO and the expression of survivin after TBI. To explore the molecular mechanism of HBO treatment effect of using the established animal models of severe traumatic brain injury, we investigated the influences of HBO on the expression of survivin after TBI.Materials and methods:The male Sprague–Dawley rats were randomly divided into three groups (n=32 for each group): sham-operated, TBI with subsequent HBOT (2ATA) , not treated after TBI . The rats were traumatized by the Feeney's brain injury model. The sham-injured animals underwent the same surgical procedure as other groups,but did not receive impact injury. The rats in HBOT group were treated respectively with HBO(0.25MPa)30minutes after TBI,and The treatments were performed every 24 hours with time length of 1 hour every time. The rats in TBI group received no additional treatments after TBI. Observing the changes of sport function, cognition function and equilibrium function,proceed the neurology point. The animals were killed at 1, 3, 5 and 7 days after TBI. Immunohistochemical method was used for detecting the expression of survivin, the results were quantitatively evaluated by image analysis. Statistical analysis was performed with the software package (SPSS 12.0). Results:The scores of behavior in HBOT group was significantly improved compared with that in TBI group (P<0.05). The expression of survivin protein was determined at 1d after TBI,and reached its peak at 7d. Neuronal localization of survivin was observed predominantly in the ipsilateral cortex and hippocampus after TBI. The masculine cells of survivin were mainly localized in neuronal endochylema. Compared to the TBI group, the number of masculine cells in HBOT group increased markedly. There was slight expression of survivin in the sham-operated group. The difference also has statistical significance.Conclusions:Survivin can express in the brain tissue after TBI. This suggests that survivin may be involved in regulation of neural cell proliferative responses after traumatic brain injury; Behavior function is improved and the expression of survivin is increased after HBOT; HBOT is an effective neuroprotective measure. The mechanism may be HBOT reduces neuronal apoptosis caused by TBI via promoting survivin expression.