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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。
Objective To investigate the content of ferritin (Fn) in various brain regions of single prolonging stress (SPS) rat model and its changes with time, and to explore the role of intracerebral ferritin in posttraumatic stress The role of PTSD in pathogenesis. Methods Sixty male adult SD rats were divided into model group (n = 35) and control group (n = 25). SPS model was established to verify whether the model was successful. The expression of ferritin in various brain regions was detected by Western blot. The expression of ferritin in hippocampus was further studied by immunohistochemistry (IHC) and real-time quantitative PCR (qRT-PCR). Western blot analysis of ferritin SPS after the trend over time. Results Compared with the control group, the behavior of the model group changed significantly (P <0.05). The expression of ferritin and gene in the model group decreased obviously and the expression of ferritin in the striatum increased significantly (P <0.05) At 1 and 3 days after stimulation, the content of ferritin in hippocampus in model group was significantly lower than that in control group (P <0.05), and recovered at 7 days. Conclusion The changes of brain ferritin in the rat model of SPS suggest that ferritin abnormalities may be involved in the pathogenesis of PTSD.