中文摘要：

目的：研究电磁辐射后大鼠海马Raf／MEK／ERK通路相关信号分子的表达变化规律。探讨辐射损伤机制。方法：分别采用X波段高功率微波（X-HPM）、S波段高功率微波（S-HPM）及电磁脉冲（EMP）模拟源辐射大鼠，建立电磁辐射动物模型。通过Western blot检测海马Raf-1、磷酸化Raf-1和磷酸化ERK的表达。结果：三种电磁辐射后6h-14d，Raf-1表达均下调，以7d最为显著，至28d基本恢复，辐射组间未见明显差异。辐射后6h和7d，磷酸化Raf-1和磷酸化ERK表达均上调，6h较为明显，磷酸化ERK的变化以两微波组更为显著。S-HPM辐射后6h～14d，磷酸化Raf-1表达持续上调，磷酸化ERK的变化呈波浪状，以6h和3d为高峰。结论：Raf／MEK／ERK信号通路参与了电磁辐射所致海马损伤；ERK通路过度活化导致神经元凋亡与坏死可能是电磁辐射致认知功能障碍的重要机制。

英文摘要：

Aim： To study the development of changes for signahng molecules related to Raf/MEK/ERK pathway in hippocampus of rats after elec- tromagnetic radiation, and investigate the mechanisms of radiation injury. Methods： Rats were exposed to X-HPM, S-HPM and EMP radiation source respectively, and animal model of electromagnetic radiation was established. Western blot was used to detect the expression of Raf-1, phosphorylated Raf-1 and phosphorylated ERK. Results： The expression of Raf-1 down-regulated during 6 h - 14 d after radiation, most significantly at 7 d, and recovered at 28 d. There was no significant difference between the radiation groups. The expression of phosphorylated Raf-1 and phusphorylated ERK beth up-regulated at 6 h and 7 d after radiation, more significantly at 6 h, and the two microwave groups were more serious for phosphorylated ERK. During 6 h- 14 d after S-HPM radiation, the expression of phosphorylated Raf-1 increased continuously, but phosphorylated ERK changed wavily, 6 h and 7 d were expression peak. Conclusion： Raf/MEK/ERK signaling pathway participates in the hippocampns injury induced by electromagnetic radiation. The excessive activation of ERK pathway may result in the apoptesis and death of neurons, which is the important mechanism of recognition disfunction caused by electromagnetic radiation.