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目的：探讨脊髓压迫性损伤白质神经纤维溃变与少突胶质细胞凋亡关系。方法采用自行设计的大鼠脊髓压迫器制作大鼠脊髓压迫性损伤模型，运用luxol fast blue（LFB）、TUNEL等方法来检测的白质神经纤维溃变及少突胶质细胞凋亡情况，采用免疫印迹技术检测蛋白Caspase-12表达变化。结果脊髓受压后，白质髓鞘化神经纤维出现水肿，排列疏松、髓鞘缺失等退行性溃变；白质少突胶质细胞凋亡数目随着脊髓压迫时间逐渐增加(P<0.05)；Caspase-12表达随压迫时间延长而上调。结论Caspase-12介导的少突胶质细胞凋亡可能参与了脊髓压迫性损伤神经纤维溃变。“,”Objective To investigate the correlation between the demyelination and apoptosis of oligodendrocyte and the mechanism of apoptosis in the compression spinal cord injury(CSCI). Methods Eighty-four adult Sprague-Dawley rats were randomly divided into 3 groups, a normal group(n=12), an operation group(n=36)and a sham operation group(n=36). The CSCI model was established with a self-made device in the operation group. The operation process in the sham operation group was the same as the operation group except the compression of spinal cord. The segments of compression spinal cord were properly taken at an interval of 1, 3 and 7 days after operation. Luxol fast blue (LFB),Immunofluorescence (IF) and TUNEL staining were performed to observe the pathological degeneration of white matters and apoptosis of oligodendrocyte. Western Blot was used to detect the expression of Caspase-12. Results LFB staining showed that the degeneration of nerve fiber occurred in the white matter and a great number of fibers were lost after compression. IF and TUNEL double staining demonstrated oligodendrocytes apoptosis occurred in spinal cord and the cell number of oligodendrocytes apoptosis increased significantly compared with the normal and sham operation group (P<0.05). Expression of Caspase- 12 also increased after compression significantly. Conclusion Demyelination occurrence and the apoptosis of oligodendrocyte may be related to the demyelination. Caspase-12 may be mediated the cell apoptosis.