摘要
目的：探讨大鼠围产期缺血缺氧脑损伤发病机制。方法：结扎Ｗｉｓｔａｒ孕鼠子宫血管，建立胎鼠缺血缺氧脑损伤模型。用原位杂交及原位末端标记法检测剖宫产后存活不同时间鼠大脑ｃｆｏｓｍＲＮＡ的表达及神经元凋亡的情况。结果：缺血后即刻大脑皮层和海马出现ｃｆｏｓｍＲＮＡ的表达，缺血后１～２ｈ和２４ｈｃｆｏｓｍＲＮＡ出现两次高表达；而对照组仅在生后１ｈ海马有较少量的表达。缺血后２ｄ神经细胞凋亡数明显多于对照组。结论：缺血缺氧引起了ｃｆｏｓｍＲＮＡ的表达增强，ｃｆｏｓ的改变可能导致其后续与细胞凋亡相关基因的转录，从而使细胞发生凋亡。
ABSTRACT Objective: To investigate the pathogenesis of cerebral injury in perinatal ischemichypoxia rat. Methods: An animal model of perinatal ischemichypoxia was set up by ligating either uterine vessel of one pregnant horn .( The adjacent horn was not ligated and those fetuses served as controls.) Pups were delivered by cesarean section at the end of the ischemichypoxic insult and then the rats' brain tissues were collected at differrent time. In situ hybridization and in situ end labeling methods were used to detect the cfos mRNA and neurons apoptosis ,respectively. Results: Our results showed that the expression of cfos mRNA in the cerebral cortex and hippocampus began immediately, peaked seperately at 12 h and 24 h after ischemichypoxic insult. Only a slight hybrid signals could be found 1 h after the delivery in hippocampus in the control group. Neuron apoptosis at 48 h after ischemichypoxia was much more than that in the control group. Conclusion: These results indicated that the expression increase of immediate early gene cfos could be induced by perinatal ischemichypoxia. The expression of cfos mRNA might induce the transcription of its target gene, especially, some “promoting apoptosis genes”, which would be a promoter for cells apoptosis.
出处
《北京医科大学学报》
CSCD
1998年第4期364-366,共3页
Journal of Peking University(Health Sciences)
基金
"九五"国家科技攻关项目
卫生部科学研究基金
