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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。
Objective: To investigate the pathogenesis of perinatal hypoxic-ischemic brain damage in rats. Methods: Uterine blood vessels of Wistar pregnant rats were ligated to establish a rat model of hypoxic-ischemic brain damage. In situ hybridization and in situ end labeling was used to detect c-fos mRNA expression and neuronal apoptosis in cortex after cesarean section at different time points. Results: The expression of c-fos mRNA in the cerebral cortex and hippocampus immediately after ischemia was observed. The expression of c-fos mRNA in the cortex and hippocampus appeared two times after ischemia, while the control group only expressed less in the hippocampus at 1 hour after birth. The number of apoptotic nerve cells in ischemic 2d group was significantly more than that in control group. Conclusion: Hypoxia-induced c-fos mRNA expression increased, c-fos changes may lead to its subsequent apoptosis-related genes transcription, so that cells apoptosis.