ABSTRACT
Objective To investigate the protective function of edaravone in the compressed spinal cord.Methods There were 150 rabbits enrolled in each group in the experiment.Rabbits in both operation group and edaravone (EDA) treating group received mild spinal cord compressionby setting a flap head screw between C6 C7 after the neck.The spinal cord decompression was conducted seven days later.After 6 hours,rabbits in the EDA treating group were injected with a large amount of EDA through ear border veins,while the rabbits in the operation group only received 0.9％ sodium chloride injection.The transmission electron microscope was used to observe the apoptotic bodies at 1 day,3 days and 7 days after compression,and 1 day,3 days,7 days,and 14 days after decompression.Flow cytometry was used to test the rate of apoptosis of spinal cord cells.Immunohistochemistry was used to test the expression of Bax protein that is related to apoptosis.Results The neuronal apoptosis appeared after compression in both operation group and EDA-treating group.The Basso Beattie Bresnahan (BBB) score,neuronal apoptosis rates,and Bax protein expressions in both groups were statistically different (P ＜ 0.05) when the spinal cord was compressed in the first day and the third day,while there was no statistically different when spinal cord compressed at the seventh day (P ＞ 0.05).After decompression of the spinal cord,the BBB score,neuronal apoptosis rates,and Bax protein expressions in both groups were becoming lower at the seventh day (P ＜0.05).Conclusions EDA has protective function for compressed spinal cord.However,only the compression of spinal cord compression period of sufficient decompression can fundamentally protect the spinal cord.