中文摘要：

目的研究单次延长刺激（single prolonging stress,SPS）大鼠模型中各个脑区铁蛋白（ferritin,Fn）含量及其随时间变化的特点,探讨脑内铁蛋白在创伤后应激障碍（posttraumatic stress disorder,PTSD）发病机制中的作用。方法将60只成年健康雄性SD大鼠分为模型组（n=35）和对照组（n=25）。建立SPS模型,采用行为学验证模型是否成功;Western blot观察大鼠各个脑区铁蛋白表达;免疫组织化学（IHC）和实时荧光定量PCR（qRT-PCR）进一步研究海马区域铁蛋白表达改变情况。Western blot观察SPS后铁蛋白随时间的变化趋势。结果与对照组相比,模型组行为发生明显改变（P〈0.05）;模型组在海马区域铁蛋白及基因表达明显减少,在纹状体区域铁蛋白表达明显增加（P〈0.05）;在应激后1、3 d,模型组海马区域铁蛋白较对照组明显减少（P〈0.05）,7 d时基本恢复。结论在SPS大鼠模型中,脑铁蛋白发生变化,表明铁蛋白异常可能参与了PTSD的发病过程。

英文摘要：

Objective To determine the changes over time of ferritin（ Fn） content in the different brain regions of rats after single prolonging stress（ SPS）,and investigate its role in the pathogenesis of posttraumatic stress disorder（ PTSD）. Methods PTSD model was established by SPS,and the model establishment was verified by behavioral test. A total of 60 healthy male SD rats were assigned into the model group（ n = 35） and normal control group（ n = 25）. Fn expression was detected in the prefrontal cortex,striatum,hippocampus and cerebellum of rats by immunohistochemistry（ IHC） and qRT-PCR. Western blotting was applied to observe the expression profile of Fn over time after SPS. Results The SPS group showed higher anxiety and fear levels（ P〈0. 05）. Fn expression was significantly decreased in the hippocampus of the SPS rats but remarkably increased in the striatum（ P〈0. 05）. The mRNA level of Fn was reduced in the hippocampus（ P〈0. 05）. In 1 and 3 d after stress,the protein level of Fn was obviously downregulated in the hippocampal region（ P〈0. 05）. Conclusion Fn expression is changed in the brain of the SPS rats,which indicating that iron metabolism abnormalities may be involved in the pathogenesis of PTSD.