分子伴侣GRP94在创伤后应激障碍大鼠前额内侧皮质表达变化及其意义

目的检测创伤后应激障碍（Post-traumatic stressdisorder，PTSD）连续单一刺激（single prolonged stress，SPS）模型大鼠前额内侧皮质（medial prefrontal cortex，mPFC）分子伴侣葡萄糖调节蛋白94（Glucose-regulated protein，GRP94）的表达变化，探讨PTSD发病机制过程中存在未折叠蛋白反应（unfolded protein reaction，UPR）的激活及GRP94在UPR中的作用机制及意义。方法健康，雄性，成年Wistar大鼠60只，建立国际认定的PTSD-SPS模型，随机分为正常对照组和模型组，模型组大鼠分别于1d、4d、7d取材。应用免疫组化、蛋白印迹和RT-PCR方法检测PTSD大鼠mPFC神经元GRP94表达变化。结果免疫组化、蛋白印迹和RT-PCR方法均显示，给予SPS刺激后大鼠GRP94的蛋白表达及GRP94mRNA表达均高于正常组（P〈O．05），7d达到顶峰。结论分子伴侣GRP94表达发生变化，提示SPS刺激后大鼠mPFC神经元出现未折叠蛋白反应的激活，PTSD的发生过程中GRP94参与了未折叠蛋白反应，对揭示PTSD致脑损伤的发病机制具有重要意义。

Changes of glucose-regulated protein 94 in medial prefrontal of rats cortex with posttraumatic stress disorder

Objective To investigate the change of glucose-regulated protein （GRP） 94 expression in the medial prefrontal cortex （mPFC） of rats under single-prolonged stress （SPS）, to determine whether GRP94 plays an important role in post-traumatic stress disorder （PTSD）, and to explore the significance and the mechanism of GRP94 expression in unfolded protein reaction. Methods A total of 60 healthy, male Wistar rats were randomly divided into a normal control group and PTSD groups of ld, 4d and 7d. SPS, an established animal model for post-traumatic stress disorder was used. We also used immunohistochemis- try, western blotting and RT-PCR to reveal the possible mechanisms induced by SPS in mPFC of PTSD rats. Results GRP94 was significantly increased in mPFC of SPS rats compared with that of the control group （P〈0. 05）, reaching the maximum at 7d. Conclusion The results indicate that the changes of GRP94 be one of the important factors in mPFC of PTSD rats. The expression suggests that unfolded pro- tein reaction is involved in PTSD, which is significant to reveal the pathogenesis.