论文部分内容阅读
背景:髓鞘蛋白是少突胶质细胞的主要成分,研究脑缺血再灌注后大脑髓鞘相关蛋白基因表达的变化有助于探讨少突胶质前体细胞在缺血性脑损伤和修复中的作用。目的:观察脑缺血再灌注后成年模型大鼠大脑髓鞘蛋白相关基因,在脑缺血后不同时间及部位表达变化和差异。方法:以线栓法制作成年SD大鼠局灶性脑缺血再灌注模型,采用5′末端标记地高辛的寡核苷酸探针荧光原位核酸分子杂交检测模型大鼠再灌注后早期大脑梗死中心区、梗死周边区和梗死对侧区皮质髓鞘蛋白脂质蛋白mRNA、髓鞘碱性蛋白mRNA和髓鞘转录因子1mRNA表达变化。结果与结论:在梗死中心区,脑缺血再灌注后早期3种髓鞘相关蛋白基因表达均明显减少;在梗死周边区,再灌注后1d时3种髓鞘相关蛋白基因表达与对照组比较无明显变化,之后逐渐增加,至14d时均高于对照组(P<0.05,0.01),以髓鞘转录因子1mRNA阳性细胞数升高最早(7d)最为显著(P<0.01)。因此,成年SD大鼠脑缺血再灌注后急性期梗死周边区皮质髓鞘相关蛋白的基因表达增加,提示少突胶质前体细胞对脑缺血性损伤敏感,其可能参与了脑缺血后损伤的修复过程。
BACKGROUND: Myelin protein is the major component of oligodendrocyte. Studying the changes of gene expression of myelin-related protein after cerebral ischemia-reperfusion is helpful to explore the role of oligodendrocyte precursor cells in ischemic brain injury and repair In the role. OBJECTIVE: To observe the changes of brain myelin protein related genes in cerebral ischemia-reperfusion model rats at different time and place after cerebral ischemia. Methods: The model of focal cerebral ischemia-reperfusion in adult SD rats was made by thread plug method. The oligonucleotide probe labeled with 5 ’end of digoxin was used to detect the early stage of reperfusion Changes of cortical myelin protein lipoprotein mRNA, myelin basic protein mRNA and myelin transcription factor 1 mRNA in the infarct center, infarct and contralateral cortex. RESULTS AND CONCLUSION: Three kinds of myelin-related protein gene expressions were significantly decreased in the infarct center and early after cerebral ischemia-reperfusion. Compared with the control group, the expression of three kinds of myelin-related protein genes in the infarct border area and at 1 day after reperfusion (P <0.05, 0.01). The number of myelin-1 mRNA positive cells increased most significantly at 7d (P <0.01). Therefore, the gene expression of myelin-associated protein in the cortex of peripheral area of adult SD rats after acute cerebral ischemia reperfusion increased, suggesting that oligodendrocyte precursor cells are sensitive to cerebral ischemic injury, which may be involved in cerebral ischemia After the injury repair process.