大鼠脊髓压迫性损伤后脱髓鞘病变及MBP、Id2的表达变化

Axonal demyelination and alteration of MBP and Id2 expression after compressed spinal cord injury

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 investigate the relationship between axonal demyelination after compressed spinal cord injury （CSCI） and expression of myelin basic protein （MBP） and inhibitor of DNA binding 2 （Id2）, and to explore the mechanism of axonal demyelination after CSCI. Methods The CSCI model was established with a self-made device. The changes of myelinated nerve fibers in white matter were determined by osmic acid staining at 1, 3 and 7 d following CSCI. MBP and Id2 expression levels were observed by double-labeling immunofluorescence and Western blotting. Results Axonal demyelination occurred after CSCI and myelin sheath became swelling, degenerative and breakdown with time extending. The expression of MBP was down-regulated after CSCI, which was consistent with the degree of demyelination. Id2 distributed widely in white matter, and its expression increased along with time extending after CSCI. Conclusion MBP and Id2 are associated with axonal demyelination, and may contribute to axonal demyelination after CSCI.