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目的建立新生鼠缺氧缺血性脑病(HIE)动物模型,阐明HIE病程中神经干细胞(NSCs)的变化特点。方法210只7日龄新生SD乳鼠随机分为正常对照组、单纯缺氧组及缺氧缺血组,每组70只。根据处死时相点每组分成3、6h,1、3、7、14、21d等7个小组,每组10只。缺氧缺血组结扎血管后左颈总动脉后置于8%氧浓度的低氧环境中2.5h,单纯缺氧组仅缺氧2.5h。采用HE、免疫组织化学染色以及光镜技术分别对3组SD大鼠脑组织中的NSCs进行检测。结果缺氧缺血后3h出现轻度脑损伤,1d病变最严重,3、7d胶质细胞增生,14、21d出现脑萎缩。3组SD大鼠脑组织均存在NSCs,从第1天开始各组间NSCs细胞数差异有统计学意义,缺氧缺血组均低于单纯缺氧组,第3天时缺氧缺血组还低于正常对照组,第7～21天单纯缺氧组高于正常对照组。3组NSCs细胞数均有显著性动态变化,趋势也基本相似,除单纯缺氧组3d高于3h和6h外,3d内各时相点差异无统计学意义;以后随着时间延长而逐渐下降,每后一时相点低于前一时相点。结论成功建立了缺氧缺血性脑病动物模型;HIE早期NSCs增殖,随着病情的演变,NSCs开始减少,最后导致病变区的NSCs相继死亡;低氧有利于NSCs的增殖。
Objective To establish an animal model of neonatal hypoxic-ischemic encephalopathy (HIE) and clarify the characteristics of neural stem cells (NSCs) during the course of HIE. Methods A total of 210 7-day-old SD neonatal SD rats were randomly divided into normal control group, hypoxia group and hypoxia-ischemia group, with 70 rats in each group. According to the point of sacrifice, each group was divided into 7 groups of 3, 6h, 1, 3, 7, 14, 21d, with 10 in each group. Hypoxic-ischemic group after the left ligation of the left common carotid artery in 8% oxygen concentration hypoxic environment 2.5h, hypoxia-only hypoxia 2.5h. HE staining, immunohistochemical staining and light microscopy were used to detect the NSCs in 3 groups of SD rats. Results Mild brain injury occurred 3 hours after hypoxia-ischemia, with the most serious lesions on day 1, glial proliferation on 3 and 7 days and brain atrophy on 14 and 21 days. NSCs were present in all three groups of SD rats. The number of NSCs in each group was statistically different from day one, and the number of NSCs in hypoxia-ischemia group was lower than those in simple hypoxia group. On the third day, Lower than the normal control group, hypoxia group was higher than the normal control group on days 7-21. The numbers of NSCs in 3 groups all had significant dynamic changes and the trends were basically the same. There was no significant difference in 3d at each time point except 3h and 6h in simple hypoxia group, and then gradually decreased with time , Each moment after the point below the previous point in time. Conclusion The animal model of hypoxic-ischemic encephalopathy was established successfully. The proliferation of NSCs in the early phase of HIE was observed. As the disease progressed, the number of NSCs began to decrease, leading to the subsequent death of NSCs in the lesion area. Hypoxia favored the proliferation of NSCs.