摘要
BACKGROUND：Studies on the immunodepressant FTY720 have primarily focused on organ transplantation and autoimmune disease therapy.However,the effects on caspase-3 expression and neural apoptosis following acute spinal cord injury remain uncertain.OBJECTIVE：To elucidate the underlying mechanism of the immunodepressant FTY720 to alleviate spinal cord injury by inhibiting expression of caspase-3 and neural apoptosis.DESIGN,TIME AND SETTING：A randomized,controlled,animal experiment was performed at Central Laboratory of the Second Affiliated Hospital of Dalian Medical University from April to July 2009.MATERIALS：FTY720 was provided by Wuhan Yuancheng Technology Developing,China.METHODS：A total of 120 Sprague Dawley rats were randomly assigned to sham-surgery,model,and FTY720 groups.Spinal cord injury at the T9-10 segment was induced in model groups using the free-fall method.Following establishment of spinal cord injury at the T9-10 segment in the FTY720 group,rats were treated with an intragastric injection of 0.3 mL saline-diluted FTY720 （3 mg/kg）.MAIN OUTCOME MEASURES：At 6,12,24,48,and 72 hours following spinal cord injury,caspase-3 expression was detected using streptavidin-peroxidase immunohistochemistry,and neural apoptosis was detected using the TUNEL method.RESULTS：Positive caspase-3 expression and neural apoptosis was not observed in the sham-surgery group at the various time points.The number of apoptotic cells increased with time after acute spinal cord injury,peaked at 24 hours following injury,and then gradually reduced.However,neural apoptosis remained at a high level.Caspase-3 expression positively correlated with neural apoptosis （r= 0.864,P〈 0.05）.Caspase-3 expression and neural apoptosis significantly decreased following FTY720 therapy （P〈 0.05）.CONCLUSION：FTY720 significantly reduced caspase-3 expression and neural apoptosis in a rat model of acute spinal cord injury.
BACKGROUND：Studies on the immunodepressant FTY720 have primarily focused on organ transplantation and autoimmune disease therapy.However,the effects on caspase-3 expression and neural apoptosis following acute spinal cord injury remain uncertain.OBJECTIVE：To elucidate the underlying mechanism of the immunodepressant FTY720 to alleviate spinal cord injury by inhibiting expression of caspase-3 and neural apoptosis.DESIGN,TIME AND SETTING：A randomized,controlled,animal experiment was performed at Central Laboratory of the Second Affiliated Hospital of Dalian Medical University from April to July 2009.MATERIALS：FTY720 was provided by Wuhan Yuancheng Technology Developing,China.METHODS：A total of 120 Sprague Dawley rats were randomly assigned to sham-surgery,model,and FTY720 groups.Spinal cord injury at the T9-10 segment was induced in model groups using the free-fall method.Following establishment of spinal cord injury at the T9-10 segment in the FTY720 group,rats were treated with an intragastric injection of 0.3 mL saline-diluted FTY720 （3 mg/kg）.MAIN OUTCOME MEASURES：At 6,12,24,48,and 72 hours following spinal cord injury,caspase-3 expression was detected using streptavidin-peroxidase immunohistochemistry,and neural apoptosis was detected using the TUNEL method.RESULTS：Positive caspase-3 expression and neural apoptosis was not observed in the sham-surgery group at the various time points.The number of apoptotic cells increased with time after acute spinal cord injury,peaked at 24 hours following injury,and then gradually reduced.However,neural apoptosis remained at a high level.Caspase-3 expression positively correlated with neural apoptosis （r= 0.864,P〈 0.05）.Caspase-3 expression and neural apoptosis significantly decreased following FTY720 therapy （P〈 0.05）.CONCLUSION：FTY720 significantly reduced caspase-3 expression and neural apoptosis in a rat model of acute spinal cord injury.
