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【目的】观察缺氧缺血(hypoxic-ischemia,HI)对人类妊娠中期胚胎脑室管膜下区(subventricular,SVZ)的影响及脑活素、神经生长因子(nerve growth factor,NGF)的神经保护作用。【方法】将5例17~22孕周人胚胎脑SVZ快速解离,行即刻培养,以氧糖缺失法建立HI损伤模型,采用析因分析,将HI组和对照组SVZ细胞按NGF、脑活素两因素,用药、不用药两个水平,交叉分成4组即刻培养。通过台盼蓝染色法观测的细胞存活率,并采用神经元特异性抗体MAP2标记神经元。【结果】SVZ神经细胞成活率在HI组为(63.41±0.06)%明显低于对照组(98.9±0.01)%(P<0.001)。HI组MAP2(+)神经元占(14.7±0.02)%明显低于对照组(48.81±0.03)%(P<0.001)。析因分析结果:HI组NGF、脑活素的主效应、交互作用均具有统计学意义(P<0.01),两药交互作用不具有统计学意义(P>0.05);而对照组两药的主效应、交互作用亦均无统计学意义(P>0.05)。【结论】妊娠中期人类胚胎脑SVZ神经细胞对HI损伤敏感。NGF和脑活素对正常神经细胞无明显影响,但可提高HI后存活的神经元数量;两药联合应用对HI损伤神经元的保护作用增强。
【Objective】 To observe the effects of hypoxic-ischemia (HI) on subventricular zone (SVZ) in human second trimester of pregnancy and the neuroprotection of cerebrolysin and nerve growth factor (NGF) effect. 【Methods】 Five SVZ cells from 17 to 22 weeks of gestational week were quickly dissociated and immediately cultured. The model of HI injury was established by oxygen-glucose deprivation. By using factorial analysis, SVZ cells in HI group and control group were treated with NGF, Surfactant two factors, medication, do not medication two levels, cross-divided into four groups immediately cultured. Cell viability was observed by trypan blue staining and neurons were labeled with neuron-specific antibody MAP2. 【Results】 The survival rate of SVZ neurons in HI group was significantly lower than that in control group (63.41 ± 0.06% vs 98.9 ± 0.01%, P <0.001). The percentage of MAP2 (+) neurons in HI group (14.7 ± 0.02)% was significantly lower than that in control group (48.81 ± 0.03)% (P <0.001). The results of factorial analysis: The main effect and interaction of NGF and cerebrolysin in HI group were statistically significant (P <0.01), and the interaction between the two drugs did not have statistical significance (P> 0.05) Main effect, interaction also had no statistical significance (P> 0.05). 【Conclusion】 SVZ neurons in human embryo during the second trimester of pregnancy are sensitive to HI injury. NGF and cerebrolysin had no significant effect on normal nerve cells, but increased the number of neurons surviving HI; the combination of the two drugs enhanced the protective effect of HI neurons.