大鼠脊髓压迫性损伤后脱髓鞘病变及MBP、Id2的表达变化

发布时间：2018-08-31 08:51

【摘要】：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。
[Abstract]:Objective to investigate the relationship between demyelinating lesions after spinal cord compression injury (compressed spinal cord injury,CSCI) and the expression of myelin basic protein (myelinbasic protein,MBP) binding inhibitor 2 (inhibitor of DNA binding2,Id2 in order to explore the mechanism of CSCI demyelination. Methods the CSCI model of SD rats was made by self-designed method. The changes of myelinated nerve fibers were detected by osmitic acid staining on the 7th day after CSCI, and the expressions of MBP and Id2 were detected by immunofluorescence double labeling and Western blot (Western blot). Results demyelinating lesions appeared after CSCI, and with the compression time prolonging, the myelin sheath gradually developed edema, degeneration and disintegration, and the expression of MBP was down-regulated after spinal cord injury. The expression trend of Id2 was consistent with the severity of demyelinating degeneration. After CSCI, Id2 was widely distributed in white matter. Conclusion the up-regulation of Id2 expression and negative regulation of the activity of MBP gene promoter and the decrease of MBP expression may be one of the mechanisms of the demyelinating lesion of nerve fiber after CSCI.
【作者单位】：重庆医科大学中医药学院;重庆医科大学神经科学研究中心;
【基金】：国家自然科学基金(30270437) 重庆市自然科学基金(CSTC2012jjA10020) 重庆市教委科学技术研究项目(KJ120312) 重庆市渝中区科技计划项目(20110316) 重庆市卫生局中医药科技项目(2012-2-138)~~
【分类号】：R341

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