少突胶质前体细胞在青老年大鼠慢性脑灌注不足中的活化改变  

Activation changes of oligodendrocyte progenitor cells during chronic cerebral hypoperfusion in young and aged rats

作　　者：叶建宁[1] 李露斯[1] 赵士福[2] 帅杰[2] 杨忠[3] 陆建华[4] 程赛宇[2] 

机构地区：[1]第三军医大学西南医院神经内科,重庆现在400038 [2]第三军医大学新桥医院神经内科 [3]第三军医大学基础部神经生物学教研室 [4]广州军区总医院麻醉科

出　　处：《中国脑血管病杂志》2007年第3期133-136,共4页Chinese Journal of Cerebrovascular Diseases

基　　金：第三军医大学留学回国人员科研启动基金资助(2004D115)

摘　　要：目的观察少突胶质前体细胞(oligodendrocyte progenitor cells,OPC)在大鼠慢性脑缺血损害中反应性变化及老化对此过程的影响。方法分别在青年(3个月龄)与老年(24个月龄)大鼠慢性灌注不足模型中,运用免疫组化方法检测NG2抗体标记的阳性OPC在灌注不足2周、1个月和3个月后形态数量及分布等改变。结果慢性灌注不足大鼠脑内存在NG2标记的免疫组化染色的阳性OPC明显反应性增生,与非缺血青老年对照组比较,差异有统计学意义(P<0.01),在皮质、皮质下、海马、胼胝体及室下区等处均有分布,以皮质下接近白质区域以及海马齿状回最为显著,2周、1个月最为明显,但于灌注不足后青年大鼠脑内NG2标记的免疫组化染色的阳性OPC染色强度和数量仍高于老年组(P<0.05)。结论慢性灌注不足过程中脑内OPC具有明显增殖活化,其反应性受月龄因素影响,并可能为慢性脑缺血损伤后的一种代偿适应或修复机制。Objective To observe the reactive changes of oligodendrocyte progenitor cells （OPC） in chronic cerebral hypoperfusion in rats and the effect of ageing on this process. Methods The changes of morphology number and distribution of OPC were detected by using neumn-glia antigen 2 （NG2） immunohistochemistry at 2 weeks, 1 month, and 3 months after cerebral hypoperfusion in the young and aged rat models. Results The rat chronic cerebral hypoperfusion models existed obvious reactive proliferation in NG2 immunohistochemistry stained OPC positive cells, as compared with the normal young and aged control groups, the differences were significant （P 〈 0. 01 ）. The cells distributed in cortex, subcortex, hippocampus, callosum, etc., particularly in subcortex near the area of white matter and the hippocampus dentate gyms, and most obviously at 2 weeks and 1 month. However, the intensity and numbers of NG2 immunohistochemistry stained OPC positive cells after cerebral hypoperfusion in the young rats were still higher than those in the aged rats （P 〈 0. 05 ）. Conclusion OPC in the brains of rats proliferate and activate obviously during the process of chronic cerebral hypoperfusion, their reactivity is affected by age factor, and may become a compensatory adaptation or repair mechanism after chronic cerebral hypoperfusion.

关 键 词：脑缺血 少突胶质前体细胞 免疫组织化学 大鼠 

分 类 号：R743.3[医药卫生—神经病学与精神病学]