| PurposeApoptosis has recently been recognized as important cell death mechanism after spinal cord injury . Methylprednisolone ,a synthethic glucocorticoid ,is the only therapeutic agent approved by Food and Drug Administration for the tre-ament of acute traumatic spinal cord injury. This study attempts to define the effect of methylprednisolone ( MP) on apoptosis of neuronal and glial cells following spinal cord injury ( SCI) and the mechanism of this effect .MethodsSixty Wistar rats were randomly devided into three groups: the MP - treated group, control group and sham group, than Forty rats with a complete transection of the thoracic spinal cord, hah0 of them received MP at half hour post - injury , half of them without received MP,animals were then sacrificed at 8, 24 h, 3 and 7 days thereafter,while the sham operation group (20 rats) were only received a laminectomy. Apoptotic cells were identified with TUNEL staining and electron microscopy in both neuronal and glial cells, the expression of Fas, caspase - 3 and Caspase - 8 were detected with the method of immunohistochemistry.ResultsThere emerged apoptotic cells at 8h after SCI , the apoptotic cells include neuronal and glial , the maximal apoptosis time is 3 days after SCI. More Fas and Caspase - 8 positive cells were present in the control group than the MP -treated group at all time points, and the differences were statistically significant(p < 0.05). Caspase-3 activity increased climax on day 7 (p < 0.05) after SCI, and there is not statistically differences between the control group and MP -treated group at all time points.ConclusionMP treated rats demonstrated a significant reduction of apoptotic cell death and a significant improvement of hind limb motor function compared with the control group rats, the reduction of apoptotic cell is associated with the inhibition of Fas and Caspase -8.
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