神经干细胞移植对注射192-IgG-saporin致AD动物模型鼠基底前脑ChAT阳性神经元的影响

目的探讨神经干细胞(NSCs)移植对注射192-IgG-saporin致老年性痴呆动物模型鼠基底前脑ChAT阳性神经元的影响。方法将24只成年SD大鼠随机分为正常组、模型组和移植组,每组8只。模型组:左侧侧脑室注射免疫毒素192-IgG-saporin2.5μg/5μL,建立192-IgG-saporin致老年性痴呆动物模型;移植组:动物模型建立后,于基底前脑行神经干细胞移植,4周后行免疫组织化学染色,结合图像分析技术观察各组大鼠基底前脑ChAT阳性神经元数量和形态学参数的变化。结果模型组注射192-IgG-saporin后1个月,观察到注射侧基底前脑内侧隔核(MS)和斜角带垂直支(VDB)ChAT阳性神经元明显减少,分别为正常组的9.70%和14.10%(与正常组相比,P<0.01);移植组ChAT阳性神经元恢复到正常组的71.51%和73.52%(与模型组相比,P<0.01)。细胞形态学参数提示,移植组ChAT阳性神经元中含有大小不等的未成熟细胞。结论神经干细胞移植对192-IgG-saporin致痴呆模型鼠基底前脑ChAT阳性神经元有明显补充和保护作用。

Effects of neural stem cell transplantation on ChAT-positive neuron in basal forebrain of AD rat induced by 192-IgG-saporin

Objective To explore the effects of neural stem cells(NSCs)transplantations on ChAT-positive neurons in basal forebrain of AD rat induced by 192-IgG-saporin.Methods Twenty-four adult SD rats were randomly divided into three groups:normal group,model group,and transplantation group,8 in each group.192-IgG-saporin(2.5 μg/5 μL)was injected into the left lateral cerebral ventricle to establish AD animal model.For the transplantation group,neural stem cells were transplanted in basal forebrain of the AD animal model above mentioned.Four weeks later,morphologic data and percentages of ChAT-positive neurons in basal forebrain were measured by immunohistochemical method combined with technique of micromeasure and image analysis.Results Immunohistochemistry showed that the number of ChAT-positive neurons in the model group were decreased to 9.70% and 14.09% of the normal group respectively in medial septum(MS)and vertical diagonal branch(VDB),and significant difference was found between the model group and normal control group(P<0.01).After the transplantation of NSCs,71.51% and 73.52% of ChAT-positive neurons were survived in MS and VDB(P<0.01,compared with the model group).Morphologic data of ChAT-positive neurons indicated that there were some premature cells among them in transplantation group.Conclusion The results suggest that ChAT-positive neurons in MS and VDB of basal forebrain of AD rats could be improved and protected by treatment with neural stem cells.