缺氧缺血性脑损伤发病中神经干细胞变化规律初探

目的：探讨缺氧缺血性脑损伤后神经干细胞(NSCs)的变化规律。方法：取新生7日SD大鼠随机分为正常对照组、缺氧组和缺氧缺血组。每组再根据处死时间点随机分成3 h,6 h,1 d,3 d,7 d,14 d,21 d 7个亚组(n=10)。缺氧缺血组大鼠分离并结扎左颈总动脉,置于密闭缺氧箱2.5 h,缺氧组不结扎血管,仅缺氧2.5 h。免疫组织化学检测海马、皮层及纹状体区阳性NSCs数。结果：正常7日龄大鼠脑组织存在NSCs,且呈明显的区域性分布,在10日龄后数目逐渐减少。缺氧组及缺氧缺血组大鼠NSCs较正常组增多,差异有显著性,在缺氧后3d(10日龄)时达高峰,后逐渐减少,缺氧组在缺氧后21 d(28日龄)时仍高于正常组。结论：H IBD发病中早期NSCs增殖;NSCs随着病情的演变开始减少;早期采用NSCs干预治疗可能为临床治疗H IBD提供重要途径。

Changes of neural stem cells following hypoxic-ischemic brain damage

Objective This study examined the changes of neural stem cells(NSCs) following hypoxic-ischemic brain damage(HIBD) in order to provide a basis for clinical use of NSCs.Methods Neonatal 7-day-old rats were randomly assigned into three groups: Normal control,Hypoxic and Hypoxic-ischemic groups.The Hypoxic-ischemic group was subjected to the left common carotid artery ligation followed by 8% oxygen exposure for 2.5 hrs.The Hypoxic group was exposed to 8% oxygen for 2.5 hrs but without the carotid artery ligation.The subjects were sacrificed at 3 and 6 hrs,and 1,3,7,14 and 21days after hypoxia/ischemia(10 rats at each time point).The number of NSCs from brain tissues of rats was detected with hematoxylin-eosin staining and immunohistochemistry.Results NSCs were presented in the normal brain tissues of neonatal rats and were reduced at 10 days postnatal.The NSCs in the Hypoxic and the Hypoxic-ischemic groups increased after hypoxia/ischemia and were significantly higher than that in the Normal control group at 6 hrs after hypoxia and at 1 day after hypoxia-ischemia.The NSCs number peaked at 3 days after hypoxia/ischemia and then decreased gradually but remained higher than that in the Normal control group at 21 days after hypoxia.Conclusions NSCs may proliferate in the early phase of HIBD but decrease while the damage is developing.Early NSCs intervention for the treatment of HIBD appears to be promising.