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机构地区:[1]南京铁道医学院附属医院儿科,南京210009
出 处:《Chinese Medical Journal》2001年第5期72-75,109,共5页中华医学杂志(英文版)
基 金:grantsfromtheScienceandTechnologyCommissionofJiangsuProvince ( 98BS5 8)andtheScienceFoundationofNationalRailwayAdministratio
摘 要:Objective To explore the mechanism of perinatal hypoxia-ischemia encephalopathy, we studied the expression of the c-fos gene and its relationship with delayed neuronal death in a rat model.Methods Cerebral hypoxia-ischemia was produced in 7-day-old SD rats using the Rice model, Reverse transcription PCR (RT-PCR), immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) were used to detect the expression of c-fos gene and cell apoptosis in the hippocampus.Results The selective expression of c-fos and delayed cell apoptosis were observed in the hypoxiaischemia hippocampus. Expression of the c-fos gene was seen in the CA4 and cingulate sulcus neurons, and apoptosis was observed in the CA1 neurons.Conclusion Transient expression of the c-fos gene may induce cerebral cell apoptosis, and may have complex relations with delayed cell death.目的 探讨围生期脑缺氧缺血后c fos基因的表达及与海马迟发性神经元死亡的相关性。方法 采用逆转录扩增、免疫组化、原位末端标记法检测脑缺氧缺血新生大鼠模型海马组织中c fos基因转录、翻译及细胞凋亡情况。结果 观察到脑缺氧缺血后海马组织中存在c fos选择性表达和迟发性细胞凋亡现象 ,且c fos基因表达以CA4、齿状回为主 ,而细胞凋亡以CA1区锥体细胞较明显。结论 围生期脑缺氧缺血后c fos基因表达参与调节了细胞凋亡的发生 。
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