论文部分内容阅读
目的 探讨新生鼠缺氧缺血再灌注后,机体神经保护机制与即刻早期基因c-fos表达的关系。方法7日龄SD鼠,经弹性管穿线阻断右颈总动脉3h,予低氧1h;制备成缺氧缺血脑损伤(HIBD)模型。后施以不同时期的再灌注,彩色多普勒监测血流阻断及再灌注情况。免疫组化观测c-fos在仔鼠HIBD后不同再灌注时间点海马的表达。Thionin染色及HE染色观测神经元的凋亡。结果 HIBD组右侧海马c-fos 6h达高峰,24h稍降,48h又升高,7d后显著降低但仍高于对照组(P<0.01)。对照组c-fos有极少数表达。凋亡检测发现:再灌注24h已有明显凋亡,7d后海马神经元未表现明显的丢失。结论c-fos可能参与HIBD后神经元的修复、存活过程;这对CA1区锥体神经元的存活非常重要。它可能经某些信号途径参与神经元的存活。
Objective To investigate the relationship between the neuroprotective mechanism and the expression of immediate early gene c-fos in neonatal rats after hypoxia-ischemia / reperfusion. Methods 7-day-old SD rats were subjected to hypoxia for 1 hour by blocking the right common carotid artery with elastic tube for 3 hours. Hypoxic-ischemic brain damage (HIBD) model was prepared. After different periods of reperfusion, color Doppler flow monitoring and reperfusion perfusion. Immunohistochemistry was used to observe the expression of c-fos in hippocampus after reperfusion in HIBD rats. Thionin staining and HE staining were used to observe neuronal apoptosis. Results The right hippocampal c-fos in HIBD group reached a peak at 6 hours, decreased slightly at 24h, increased at 48 hours, decreased significantly at 7 days and still remained higher than that of the control group (P <0.01). Control group c-fos a very small number of expression. Apoptosis detection found: 24 h reperfusion has been significantly apoptosis, hippocampal neurons did not show significant loss after 7 days. Conclusions c-fos may participate in the repair and survival process of neurons after HIBD, which is very important for the survival of pyramidal neurons in CA1 area. It may participate in the survival of neurons through some signaling pathways.