创伤后应激障碍大鼠海马神经元凋亡中Caspase-12的表达  

Expression of Caspase-12 in cellular apoptosis of hippocampus in the rat model of posttraumatic stress disorder

作　　者：刘虹[1] 韩芳[1] 石玉秀[1] 

机构地区：[1]中国医科大学基础医学院组织学与胚胎学教研室,沈阳110001

出　　处：《解剖学报》2014年第4期452-456,共5页Acta Anatomica Sinica

基　　金：国家自然科学基金资助项目(81171282)

摘　　要：目的观察创伤后应激障碍(PTSD)大鼠海马神经元凋亡和Caspase-12表达的变化。方法采用单一延长应激(SPS)方法刺激大鼠建立PTSD模型,健康雄性Wistar大鼠随机分为SPS 1d、4d、7d组和正常对照组。应用透射电子显微镜观察PTSD大鼠海马神经元的形态学改变,采用免疫组织化学、免疫印迹法和RT-PCR技术检测海马神经元Caspase-12表达的变化。结果 SPS后,海马神经元发生了凋亡的形态学改变,Caspase-12的表达于刺激后4d最多。结论 PTSD激活凋亡因子Caspase-12启动海马神经元经内质网途径细胞凋亡,可能是PTSD患者海马萎缩的一个病理生理学基础。Objective To observe changes of apoptosis and Caspase-12 expression in hippocampus of the rat model of posttraumatic stress disorder （ PTSD ） .Methods Single prolonged stress （ SPS ） was used to duplicate a rat model of PTSD.Male Wistar rats were randomly divided into 1, 4, 7 days groups after exposure to SPS and a normal control group.Transmission electron microscopy was used to observe morphologic changes of the hippocampus neurons .The expression of Caspase-12 was detected by immunohistochemistry , Western blotting and RT-PCR.Results After SPS, the hippocampus neurons had characteristic morphologic changes of apoptosis , and the expression of Caspase-12 reached the peak at SPS 4d.Conclusion PTSD activates the ERS-mediated apoptosis in hippocampus via Caspase-12, which may be a pathophysiology base of the atrophy of the hippocampus in PTSD .

关 键 词：创伤后应激障碍 海马 神经元 免疫印迹法 大鼠 

分 类 号：R329.4[医药卫生—人体解剖和组织胚胎学]