中文摘要：

目的 观察Caspase-9、Caspase-3和细胞色素C（CytC）在创伤后应激障碍（PTSD）大鼠海马神经元中的表达及相互关系，探讨PTSD大鼠海马神经元凋亡的信号转导机制。 方法 成年雄性Wistar大鼠60只，采用国际认定的无连续单一应激（SPS）方法刺激大鼠建立PTSD大鼠模型，取SPS刺激后1d、4d、7d、14d、28d 组和正常对照组。应用免疫组织化学、免疫荧光和免疫印迹法检测Caspase-9、Caspase-3和CytC蛋白的表达。 结果 免疫组织化学和免疫荧光结果显示，CytC蛋白于SPS刺激后4 d在海马神经元胞质内的表达达到高峰，并维持较高水平，SPS刺激后7d逐渐下降。SPS刺激后，Caspase-9和Caspase-3阳性表达增强，均于SPS刺激后7d达到高峰。免疫印迹结果显示，与正常对照组相比，模型组海马胞质内CytC蛋白水平明显上调，于SPS刺激后4 d达到较高水平。而SPS刺激后线粒体中CytC蛋白水平则显著下降。在正常对照组，无Caspase-9和Caspase-3活性片段；在模型组，出现Caspase-9和Caspase-3活性片段，两者均于SPS刺激后7d达到高峰，14 d开始下调。 结论 神经元凋亡可能是导致PTSD大鼠海马萎缩的重要机制之一；线粒体通路的激活参与了PTSD大鼠海马神经元凋亡的调控。

英文摘要：

Objective To observe the expressions of Caspase-9,Caspase-3, cytochrome C and their relationships, and investigate apoptotic mechanisms in hippocampus of posttraumatic stress disorder（PTSD） rats. Methods Sixty male Wistar rats were used in the present study. The singleprolonged stress （SPS）method was used to set up the rat PTSD models. There were six groups：after SPS 1 day,4 days,7 days,14 days,28 days groups and control group. The expressions of Caspase-9, Caspase-3 and Cytochrome C proteins were detected with immunohistochemistry, immunofluorescence and Western blotting. Results Immunohistochemical and immunofluorescent results showed that the expression of cytochrome C peaked at 4 days and maintained higher level at 7days after SPS. Expressions of Caspase-9 and Caspase-3 were increased and peaked at 7days after SPS. Western blotting results showed that compared with control group, cytochrome C protein was upregulated and peaked at 4 days after SPS in the cytosol. Compared with the control group, cytochrome C tended to decrease in mitochondrial fractions. The activated form of Caspase-9 and Caspase-3 were not detected in control group. They were present in model groups. Cleaved Caspase-9 and cleavedCaspase-3 peaked at 7 days after SPS, and then gradually decreased at 14 days. Conclusion The neuronal apoptosis in hippocampus of PTSD rats may be one of the causes inducing hippocampus atrophy. Mitochondrial apoptotic pathway is involved in apoptosis in the hippocampus of PTSD rats.