目的 探讨右美托咪定（DEX）对创伤后应激障碍大鼠（PTSD）核因子κB抑制蛋白激酶（IKK）/核因子κB抑制蛋白α（IκBα）/核因子κB（NF-κB）通路及认知功能障碍的影响。  方法 将大鼠按照随机数字表法分为空白对照（control）组、模型（model）组、阳性对照（positive）组和DEX组。除control组外，其余各组使用单一延长应激法（SPS）构建PTSD模型，并于模型制作后分别给予相应药物。旷场实验和Morris水迷宫法检测大鼠自主活动和学习记忆能力；HE染色法观察大脑皮层和海马组织病理变化；ELISA和Western blotting检测海马组织白细胞介素（IL）-1β、IL-6和肿瘤坏死因子α（TNF-α）含量及IKK、IκBα、嘌呤能离子通道型受体7（P2X7R）和富含亮氨酸重复结构域蛋白3（NALP3）表达水平；凝胶电泳迁移率转变分析（EMSA）评价NF-κB活性。  结果 与control组相比，model组大鼠大脑皮层及海马CA1区出现结构紊乱，细胞核固缩等病理变化，大鼠自主活动和学习记忆能力降低（P<0.05）， IL-1β、IL-6和TNF-α含量、IKK、IκBα、P2X7R和NALP3表达水平及NF-κB活性升高（P<0.05）；与model组相比，positive组和DEX组大鼠大脑皮层及海马CA1区病理现象缓解，上述指标变化均与model组相反（P<0.05）。  结论 DEX可显著提高PTSD大鼠自主活动和学习记忆能力，减少海马组织炎症反应，改善认知功能障碍，可能与下调IKK/IκBα/NF-κB通路有关。

Objective To investigate the effects of dexmedetomidine (DEX) on the nuclear factor-κB inhibitor protein kinase (IKK)/nuclear factor-κB inhibitor protein α (IκBα)/nuclear factor-κB (NF-κB) pathway and cognitive dysfunction in rats with post-traumatic stress disorder (PTSD).   Methods Rats were randomly divided into control group, model group, positive group and DEX group. Except for the control group, the PTSD model was constructed by single prolonged stress method  (SPS), and the corresponding drugs were given after the completion the model. Open field test and Morris water maze method  were used to detect the autonomous activity, learning and memory ability of rats; HE staining was used to observe the morphological characteristics of cerebral cortex and hippocampus; ELISA and Western blotting were used to detect the contents of interleukin (IL)-1β, IL-6, tumor necrosis factor α(TNF-α) and the expression levels of IKK, IκBα, purinergic ligand-gated ion channel 7 receptor (P2X7R), leucine-rich repeat domain protein 3(NALP3) in hippocampus; the NF-κB activity was assessed by electrophoretic mobility shift assay (EMSA).   Results Compared with the control group, the cerebral cortex and hippocampal CA1 region of model group were in structural disorders, nuclear pyysis and other pathological changes happend, learning and memory ability of rats decreased(P<0.05), contents of IL-1β, IL-6 and TNF-α, expression levels of IKK, IκBα, P2X7R and NALP3, NF-κB activity in hippocampus increased(P<0.05); Compared with the model group, the pathological phenomena in cerebral cortex and hippocampal CA1 area of rats in positive group and DEX group were in alleviated, and the changes of the above indexes were opposite to those of model group(P<0.05).   Conclusion DEX can significantly improve the autonomous activity ability and learning and memory ability in PTSD rats, reduce inflammatory reaction in hippocampus and improve cognitive dysfunction, which may be related to the down-regulation of IKK/IκBα/NF-κB pathway.