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目的观察新生鼠缺氧缺血损伤后内源性神经干细胞的增殖及迁移。方法制成新生鼠缺氧缺血脑损伤模型,采用单、双标免疫组织化学方法检测5溴脱氧尿苷(BrdU)和巢蛋白(Nestin)的表达。BrdU标记增殖的新生细胞,Nestin标记神经干细胞。结果正常新生鼠生后保持较短一段时间的增殖活跃,生后3d达高峰,7d后逐渐减弱,生后21d后形成与成年动物相似的发生模式。缺氧缺血损伤后,细胞增殖恢复活跃,BrdU阳性细胞数于伤后4d达高峰,皮层、纹状体、海马可见散在阳性细胞,大多数BrdU阳性细胞集中位于室管膜下区的背外侧角及外侧壁处,伤后7d后逐渐减少,21d更多的BrdU阳性细胞迁移至损伤区;损伤后Nestin阳性细胞数增加,同时一定数量的Nestin阳性细胞由G0期进入增殖周期。结论缺氧缺血脑损伤可刺激新生鼠内源性神经干细胞的增殖及迁移。
Objective To observe the proliferation and migration of endogenous neural stem cells after hypoxic-ischemic injury in neonatal rats. Methods The hypoxic-ischemic brain damage model was made in neonatal rats. The expression of BrdU and Nestin were detected by single and double immunohistochemistry. BrdU labeled proliferation of newborn cells, Nestin labeled neural stem cells. Results The normal neonatal rats maintained a relatively short proliferative activity after birth, peaked at 3 days after birth, and gradually weakened after 7 days. The pattern of occurrence similar to that of adult animals was found 21 days after birth. Hypoxic-ischemic injury, cell proliferation was restored, the number of BrdU positive cells peaked 4d after injury, cortex, striatum, hippocampus scattered positive cells, most of the BrdU positive cells located in the dorsolateral subventricular zone Angle and lateral wall. The numbers of BrdU positive cells migrated to the lesion after 21 days, and the number of Nestin positive cells increased after injury. Meanwhile, a certain number of Nestin positive cells entered the proliferative cycle from G0 stage. Conclusion Hypoxic-ischemic brain damage can stimulate the proliferation and migration of endogenous neural stem cells in neonatal rats.