Autologous transplantation of neural stem cells in neonatalhypoxic ischemic brain injury in rats

本研究从新生大鼠缺氧缺血性脑损伤后3天的缺血区获得了有丝分裂能力较强的神经干/神经前体细胞。然而，由于从新生儿脑组织中抽吸缺血组织，导致MRI图像上缺血病变的扩大和运动功能测试的恶化，因此，我们将本研究的治疗方法从自体移植改为增强脑室下区(SVZ)内固有的神经干/神经前体细胞(SVZ)和脑室内注射通常采用的神经球培养方法中的EGF和FGF。此方法可导致下丘脑室旁带、结缔组织下缘及缺血灶周围的BrdU标记细胞增多。缺氧缺血后7d脑组织组织学观察，几乎所有BrdU标记细胞分别与神经前体细胞DCX、星形胶质细胞标记GFAP和少突胶质细胞前体O4双标，因此BrdU标记细胞在本研究中似乎仍处于未分化阶段。

In this study, neural stem/neural progenitor cells with strongmitotic ability were obtained from the ischemic brain lesion at 3 says after neonatalhypoxic ischemic insult in rats. However, aspiration of ischemic tissue from neonatalbrain led to expand of ischemic lesions on MRI image and worsen of motor function test.Therefore, we changed the therapeutic method of this study from autologoustransplantation to enhancement intrinsic neural stem/ neural progenitor cells in thesubventricular zone (SVZ) and ischemic lesions with intraventricular injection of EGFand FGF which were usually used on neurosphere culture method. This method led to increasebromodeoxyuridine (BrdU) labeled cells in the SVZ, lower edge of corpus callosum andaround of ischemic lesion. Histological investigation of brain tissue at 7days afterhypoxia ischemia, almost all BrdU labeled cells were double labeled with neural progenitormaker DCX, astrocyte maker GFAP and oligodendrocyte progenitor maker O4, respectively.Therefore, BrdU labeled cells were seemed to still undifferentiated stage in thisanalysis.