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

本研究从大鼠新生儿缺氧缺血性损伤后3周的缺血性脑损伤处获得具有强有丝分裂能力的神经干/神经祖细胞。然而，从新生儿脑中抽取缺血组织导致MRI图像上缺血性病变扩大，运动功能检查恶化。因此，我们将本研究的治疗方法从自体移植改为脑室内注射egf和FGF增强脑室下区（SVZ）和缺血性病变的固有神经干/神经祖细胞，这是通常用于神经球培养方法的。该方法导致SVZ、胼胝体下缘和缺血性病变周围BrdU标记细胞增多。缺氧缺血后7d脑组织组织学观察，BrdU标记的细胞几乎全部分别用神经祖细胞制造物DCX、星形胶质细胞制造物GFAP和少突胶质细胞祖细胞制造物O4进行双标记。因此，在本分析中，BrdU标记的细胞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.