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.
ABSTRACT
BACKGROUND:Dexamethasone can improve the cellapoptosis and decrease the number of osteoblasts and bone cells through increasing the time of cellcycle. Protein kinase C is a kind of intraecellular singnal transduction pathways, and there are related reports on the relationship between protein kinase C and cellapoptosis. OBJECTIVE:To investigate the mechanism of dexamethasone-induced osteoblast apoptosis via protein kinase C intracellular signal transduction pathway. METHODS:Fetal rat bone marrow mesenchymal stem cells were col ected for osteogenic induction, and the cells were divided into dexamethasone group, phorbol group and star cytochalasin group. The cells in the dexamethasone group were added with 1×10-6 mol/L dexamethasone, the cells in the phorbol group were added with 1×10-6 mol/L dexamethasone and 1×10-7 mol/L phorbol, while the cells in the star cytochalasin group were added with 1×10-6 mol/L dexamethasone and 1×10-7 RESULTS AND CONCLUSION:Dexamethasone could induce apoptosis significantly, and after added with mol/L star cytochalasin. The proliferation and inhibition of the cells in different intervention groups were observed, and the content of protein kinase C in the cellmembrane and cytoplasm was measured. phorbol, the apoptosis was increased significantly;while after added with star cytochalasin, the apoptosis was decreased significantly. After added with dexamethasone, the content of protein kinase C in the cytoplasm was significantly decreased, while increased in the cellmembrane. At different time points after added with dexamethasone, the change of the content of protein kinase C in the cytoplasm and cellmembrane was most significant at 30 minutes. The results indicated that mechanism of dexamethasone-induced osteoblast apoptosis was correlated with protein kinase C, and dexamethasone was the agonist of protein kinase C. After the cells were stimulated, the protein kinase C in the cytoplasm wil moved to the cellmembrane, and then the content of protein kinase C in the cytoplasm was decreased, while increased in the cellmembrane.