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为探讨围产期缺血缺氧脑损伤的发病机制，本实验对c-fos在脑缺血缺氧后的表达变化规律进行了研究。通过结扎Wistar孕鼠一侧子宫角血管的方法（未结扎侧子宫角作为对照），建立围产期缺血缺氧脑损伤动物模型。采用原位杂交方法观察了剖宫产后存活不同时间的大鼠大脑c-fosmRNA的表达，结果发现，缺血后即刻，大脑皮层和海马即出现c-fosmRNA的表达。随时间延长，表达量逐渐增加，至1h时，杂交信号最强，维持到2、4h后逐渐减弱。但到24h时.c-fosmRNA又出现第二次高表达，以后又逐渐减低，48h表达极微，3d后各组都未检出其表达。对照组仅在生后1h海马有较少量c-fosRNA的表达。结果表明，宫内缺血缺氧引起了即刻早期基因c-fosmRNA的表达增强，且具有一定规律性。c-fos的改变可能会引起其后续靶基因尤其是一些与细胞死亡相关基因的转录，从而引起脑组织的病理损害。
In order to investigate the pathogenesis of perinatal hypoxic-ischemic brain damage, we studied the expression of c-fos after cerebral ischemia and hypoxia. Animal model of perinatal hypoxic-ischemic brain damage was established by ligating the uterine horn blood of one side of Wistar pregnant mice (uterine horn without ligation). In situ hybridization was used to observe the expression of c-fos mRNA in the rat brain after cesarean section. The results showed that the expression of c-fos mRNA appeared in the cortex and hippocampus immediately after ischemia. With the extension of time, the expression increased gradually, and at 1h, the hybridization signal was the strongest, and gradually decreased after 2 h. However, by 24 h, c-fos mRNA appeared a second high expression, and then gradually decreased after 48 h expression was extremely small, 3d after the group did not detect its expression. The control group only had a small amount of c-fosRNA expression in the hippocampus at 1 hour after birth. The results showed that intrauterine ischemia and hypoxia caused immediate early gene c-fos mRNA expression increased, and has a certain regularity. Changes in c-fos may cause subsequent target genes, especially those associated with cell death, to cause pathological damage in brain tissue.