| Objective:To study the effects of free radical scavenger (edaravone) and ultrashort wave on neuroprotection and neural plasticity in traumatic brain injury in rats. Moreover, the mechanisms and synergistic actions were investigated.Methods:The model of traumatic brain injury in rats were established by a free-failing body device. The rats were divided into 5 groups:edaravone group, ultrashort wave group, ultrashort wave combined with edaravone group, trauma control group, blank control group. The manifestations of the rats in different group during the processes were observed and the expression changes of rat brain's ionotropic receptors NMDAR1 and GAP-43 were determined by immunohistochemical method at different time points:1d,3d,7d and 14d.Results:Compared with the trauma control group, the expression of NMDAR1 in three groups were down-regulated (P<0.05) but the expression of GAP-43 was no significant difference. The expression of NMDAR1 and GAP-43 were up-regulated in the three groups at 3d,7d and 14d (P<0.05), except the expression of NMDAR1 in edaravone group (P>0.05). Generally, there was no significant difference among the three groups. Conclusion:Early free radical scavenger therapy and timely ultrashort wave therapy could help to reduce the brain edema and inhibit neuronal apoptosis, promote the reconstruction of nerve synapses and the recovery of the learning and memorizing ability. There was no significant difference between the two therapys in curative effectiveness. |
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