首页> 中文期刊> 《中国组织工程研究》 >短暂脑缺血后老年模型大鼠大脑少突胶质前体细胞的变化

短暂脑缺血后老年模型大鼠大脑少突胶质前体细胞的变化

         

摘要

BACKGROUND: At present, it is not yet clear about the alteration of oligodendrocyte precursor cells after transient cerebral ischemic and in the repair process.OBJECTIVE: To investigate the alteration of oligodendrocyte precursor cells in aged rats after transient cerebral ischemia. METHODS: A rat model of transient cerebral ischemia was established by thread embolism methods. Twenty-four aged male SD rats were randomly divided into four groups: control group, days 1, 7 and 14 after ischemia-reperfusion groups. Rats in the control group were only subjected to an exposed blood vessel and sutured with no embolism. Rats in the ischemia-reperfusion groups were subjected to reperfusion for 1, 7 and 14 days after model establishment.RESUTS AND CONCLUSION: ①Compared with the control group, the number of cells positive for chondroitin sulfate proteoglycan, unmature oligodendrocyte marker and 2',3'-cyclic nucleotide 3'-phosphodiesterase in the infarction core was significantly decreased at each time point after transient cerebral ischemia. ② In peri-infarction area, the number of cells positive for chondroitin sulfate proteoglycan and unmature oligodendrocyte marker was increased gradually with time, which was increased dramatically at days 7 and 14 after transient cerebral ischemia. While, the number of 2',3'-cyclic nucleotide 3'-phosphodiesterase-positive cells was decreased slightly at days 1 and 7 after transient cerebral ischemia. ③There was no significant difference among the number of the three kinds of antigen positive cells in the contralateral cerebral infarction area. These findings suggest that the number of oligodendrocyte precursor cells is increased in the peri-infarcted area after transient cerebral ischemia in aged SD rats. The cells may differentiate into mature cells and participate in the repair of cerebral ischemia injury.%背景:目前老年脑内少突胶质前体细胞在短暂脑缺血后和修复过程中的变化尚不清楚.目的:观察短暂脑缺血后老年模型大鼠大脑少突胶质前体细胞的变化.方法:以线栓法制作大鼠短暂脑缺血模型,24只12月龄老年雄性SD大鼠随机数字表法分4组,对照组仅暴露血管,然后缝合,不进行栓塞;缺血再灌注1,7,14 d组:造模后分别再灌注1,7,14 d.结果与结论:①短暂脑缺血后各时间点梗死中心区硫酸软骨素蛋白聚糖、未成熟少突胶质细胞的标记物(O4)和环核苷酸磷酸二酯酶阳性细胞数明显减少.②梗死周边区硫酸软骨素蛋白聚糖和O4阳性细胞数随着时间延长而逐渐增加,短暂脑缺血后7,14 d时显著增加;而环核苷酸磷酸二酯酶阳性细胞数在短暂脑缺血后1,7 d时稍有减少,脑缺血后14 d时明显增加.③脑梗死对侧区3种抗原阳性细胞数无明显变化.提示老年SD大鼠短暂脑缺血后梗死周边区少突胶质前体细胞增多,并可能分化为成熟少突胶质细胞,参与脑缺血损伤的修复过程.

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