过表达Olig2的少突胶质前体细胞在缺血缺氧脑白质损伤新生大鼠脑内的分化
发布时间:2018-06-03 05:08
本文选题:缺血缺氧 + 脑白质损伤 ; 参考:《神经解剖学杂志》2017年06期
【摘要】:目的:观察过表达特异性转录因子Olig2的少突胶质前体细胞(oligodendrocyte precursor cells,OPCs)移植在缺血缺氧(hypoxia-ischemia,HI)脑白质损伤新生大鼠脑内的分化情况。方法:用绿色荧光蛋白(green fluorescent protein,GFP)标记的过表达Olig2的慢病毒感染原代分离纯化的大鼠大脑皮层OPCs,GFP阳性细胞计数测其感染率。将过表达Olig2的OPCs(Olig2组)或阴性对照病毒感染的OPCs(Vector组)脑立体定位注射到造模后7 d的HI模型大鼠胼胝体膝部,移植后2周,冰冻切片行免疫荧光染色观察OPCs的存活和分化情况。结果:Olig2-GV218病毒感染OPCs细胞48 h,荧光显微镜检测显示85%左右的OPCs细胞表达GFP;移植后2周,caspase-3荧光染色表明移植后绝大部分细胞存活,Vector组和Olig2组之间无统计学差异(P0.05);GFAP/GFP双阳性细胞在两组之间也无显著差异(P0.05);而Olig2组MBP/GFP双阳性细胞的荧光密度显著高于Vector组(P0.05)。结论:过表达Olig2可促进移植OPCs向少突胶质细胞分化。
[Abstract]:Aim: to observe the differentiation of oligodendrocyte precursor cells with oligodendrocyte precursor cells in the white matter injury of neonatal rats after ischemia and hypoxia. Methods: the infection rate of lentivirus labeled with green fluorescent protein (GFP) was determined by primary isolation and purification of GFP positive cells from rat cerebral cortex. The rats were injected into the knees of corpus callosum of HI model rats 7 days after transplantation. The survival and differentiation of OPCs were observed by immunofluorescence staining in frozen sections 2 weeks after transplantation. Results at 48 h after infection with OPCs cells, about 85% of OPCs cells were detected by fluorescence microscopy, and 2 weeks after transplantation, there was no significant difference between the survival vector group and Olig2 group in the survival of most of the cells, and there was no significant difference between the two groups (P0.05GFP / GFAP / GFP). There was no significant difference in sex cells between the two groups, while the fluorescence density of MBP/GFP double positive cells in Olig2 group was significantly higher than that in Vector group. Conclusion: overexpression of Olig2 can promote the differentiation of OPCs into oligodendrocytes.
【作者单位】: 徐州医科大学机能学实验中心;徐州医科大学神经生物学研究中心;
【基金】:国家自然科学基金(81271345)
【分类号】:R742
,
本文编号:1971587
本文链接:https://www.wllwen.com/yixuelunwen/shenjingyixue/1971587.html
最近更新
教材专著