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目的分析脊髓压迫性损伤(compressed spinal cord injury,CSCI)后脱髓鞘病变与髓鞘碱性蛋白(myelinbasic protein,MBP)、DNA结合抑制物2(inhibitor of DNA binding2,Id2)的表达变化之间的关系,以探讨CSCI脱髓鞘病变机制。方法采用自行设计的方法制作SD大鼠CSCI模型,通过锇酸染色检测CSCI后1、3、7 d有髓神经纤维变化;运用免疫荧光双标和免疫印迹(Western blot)检测MBP及Id2的表达变化。结果 CSCI后出现脱髓鞘病变,并随着压迫时间延长,髓鞘逐渐发生水肿、变性、崩解;脊髓损伤后MBP表达下调,其表达趋势与脱髓鞘溃变的严重程度一致;CSCI后,Id2广泛分布于白质,随着压迫时间延长,其表达逐渐上调。结论 Id2表达上调,并负向调控MBP基因启动子的活性,使MBP的表达下降,是CSCI后神经纤维脱髓鞘病变的机制之一。
Objective To analyze the relationship between the changes of demyelinating lesions and the expression of myelin basic protein (MBP) and inhibitor of DNA binding 2 (Id2) after compressed spinal cord injury (CSCI) In order to investigate the mechanism of CSCI demyelination. Methods SD rat model of CSCI was established by self-designed method. The changes of myelinated nerve fibers on 1, 3 and 7 days after CSCI were detected by osmium tetroxide staining. The expressions of MBP and Id2 were detected by immunofluorescence double-labeled and Western blotting Variety. Results The demyelinating lesions occurred after CSCI. With the extension of compression time, myelin gradually developed edema, degeneration and disintegration. MBP expression was down-regulated after spinal cord injury, and the expression tendency was consistent with the severity of demyelinating degeneration. After CSCI , Id2 is widely distributed in white matter, with the oppression of time extended its expression gradually increased. Conclusions Id2 expression is up-regulated and the activity of MBP gene promoter is negatively regulated, thus decreasing the expression of MBP, which is one of the mechanisms of demyelinating lesions of nerve fibers after CSCI.