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目的探讨短暂缺氧对新生鼠脑神经源性分化因子(NeuroD)表达以及细胞凋亡和神经再生的影响。方法新生10～24h的SD大鼠短暂置于100%氮气环境中,建立出生窒息模型。96只新生大鼠随机分为对照组、缺氧20min组,其中1个亚组分3个时间点(13、20、27d)取材,采用免疫荧光法检测NeuroD、免疫组织化学法检测5-溴脱氧尿嘧啶核苷(BrdU)表达的变化。另一亚组分2个时间点(6、20d)取材,原位缺口末端标记法(TUNEL)检测细胞凋亡。结果免疫荧光/免疫组织化学结果显示,缺氧20min组13、27d NeuroD和BrdU在海马CA1区/室下区的表达量均高于对照组(P<0.05),且在20d表达量最高(P<0.01)。TUNEL法检测出缺氧20min后6d在海马CA1区凋亡细胞阳性率明显高于对照组(P<0.01),而20d凋亡细胞阳性率与对照组比较差异无统计学意义。结论缺氧引起迟发性细胞凋亡,导致神经元缺失,可能诱导细胞增殖、分化,触发神经发生,对受损的脑组织进行代偿性修复和神经功能重建。
Objective To investigate the effect of transient hypoxia on the expression of NeuroDifferentiation factor (NeuroD), apoptosis and neural regeneration in neonatal rats. Methods Newborn SD rats aged 10 ~ 24h were placed in 100% nitrogen atmosphere for a short time to establish a model of asphyxial birth. 96 neonatal rats were randomly divided into control group, hypoxia 20min group, of which 1 sub-component at three time points (13,20,27 d) were drawn, NeuroD was detected by immunofluorescence, 5-Br Changes of deoxyuridine (BrdU) expression. The other sub-component was taken at two time points (6 and 20 days), and apoptosis was detected by TUNEL. Results The results of immunofluorescence and immunohistochemistry showed that the expression of NeuroD and BrdU in hippocampal CA1 region / subventricular zone at 13 and 27 days after hypoxia was higher than that in control group (P <0.05) <0.01). The positive rate of apoptotic cells in hippocampal CA1 area at 6th day after hypoxia was detected by TUNEL method was significantly higher than that of control group (P <0.01), while the positive rate of apoptotic cells at 20d was not significantly different from that of control group. Conclusion Hypoxia causes delayed apoptosis and leads to the loss of neurons. It may induce cell proliferation and differentiation, trigger neurogenesis, compensate compensatory repair and neurological reconstruction of impaired brain tissue.