摘要
目的:研究cjun与FasmRNA在胎鼠缺血缺氧后脑内的表达关系,探讨围生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。用原位杂交检测剖宫产娩出后存活不同时间大鼠大脑cjunmRNA及FasmRNA的表达。结果:缺血后15min,大脑皮层和海马即出现cjunmRNA的表达,缺血后1~2h和24h,cjunmRNA出现两次高表达;而缺血后1h,FasmRNA在大脑皮层和海马出现表达,4h和48h出现两次表达高峰。结论:缺血缺氧引起了cjun及FasmRNA的表达增强,cjun的表达增加可能是Fas高表达的信号通路之一。
Objective: To study the expression relationship between c jun mRNA and Fas mRNA for further investigating the pathogenesis of cerebral injury in perinatal ischemic hypoxia. Methods: An animal model of perinatal ischemic hypoxia 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 ischemic hypoxic insult and then the rats' brain tissues were collected at differrent time points. In situ hybridization was used to detect the c jun mRNA and Fas mRNA separately. Results: The expression of c jun mRNA began at 15 min in cerebral cortex and hyppocampus, peaked separately at 1-2 hours and 24 hours after ischemic hypoxic insult. However, the Fas mRNA expression began at hour 1 in cerebral cortex and hyppocampus , peaked separately 4 hours and 48 hours after the insult. Conclusion: The increase expression of c jun and Fas mRNA could be induced by perinatal ischemic hypoxia. The expression of c jun mRNA might be one of the signal pathways for the Fas mRNA higher expression following perinatal ischemic hypoxia.
出处
《北京医科大学学报》
CSCD
1998年第5期460-462,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
关键词
脑缺血
遗传学
脑缺氧
遗传学
FAS基因
Cerebral ischemia/genet Cerebral anoxia/genet Fas gene ☆ Genes, jun/metab