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目的:探讨迷走神经电刺激(VNS)对创伤性脑损伤(TBI)大鼠行为学及α7烟碱型乙酰胆碱受体(α7 nAChR)、炎性因子表达的影响。方法:72只雄性SD大鼠按随机数字表法分为假手术组、TBI组、VNS组，每组24只。后2组大鼠采用改良式自由落体法制备成中度TBI模型(假手术组暴露硬脑膜但不撞击)，且VNS组造模后连续14 d给予VNS(频率30 Hz、脉宽100 μs、电流0.8 mA、刺激5 min、停止5 min，反复进行3次)。造模后第1、3、7、14、21、28天采用平衡木平衡及行走实验评估各组大鼠的神经功能；造模后第24~28天采用水迷宫实验评估各组大鼠的空间学习记忆能力；造模后第28天取各组大鼠的脑组织切片计算脑损伤灶体积；造模后第14天采用Nissel染色观察各组大鼠脑损伤区周围的神经元形态及生存情况，免疫组化染色观察海马齿状回及CA3区的神经核抗原(NeuN)阳性神经元数量，酶联免疫吸附法检测炎性因子白介素(IL)-1β、IL-6、肿瘤坏死因子(TNF)-α、核因子-κB(NF-κB)的表达水平；造模后第3、7、14天采用Western blotting法检测各组大鼠脑损伤区中α7 nAChR蛋白的表达水平。结果:与TBI组比较，VNS组造模后第7、14、21、28天的平衡木平衡时间明显延长，平衡木行走时间明显缩短；造模后第27、28天的逃避潜伏期明显缩短，目标象限探索时间明显延长；造模后第28天的脑损伤体积明显减小；造模后第14天的脑损伤区周围Nissel染色阳性神经元数量明显增多，海马齿状回及CA3区NeuN阳性神经元数量明显增多，IL-1β、IL-6、TNF-α、NF-κB表达水平明显降低；造模后第7、14天的脑损伤区中α7 nAChR蛋白表达水平明显升高，差异均有统计学意义(n P<0.05)。n 结论:VNS能够促进TBI大鼠的行为学恢复，其机制与上调α7 nAChR蛋白表达，降低炎性因子IL-1β、IL-6、TNF-α、NF-κB释放有关。“,”Objective:To investigate the effect of vagus nerve stimulation (VNS) on α7 nicotinic acetylcholine receptor (α7 nAChR) and inflammatory factor expressions and behavioristics in rats after traumatic brain injury (TBI).Methods:Seventy-two male Sprague-Dawley rats were randomly divided into sham-operated group, TBI group and VNS group (n n=24). The TBI models in the latter two groups were established by modified weight drop method; the dura mater in the sham-operated group was exposed without impingement. The VNS group received VNS treatment for 14 consecutive d (frequency: 30 Hz, pulse width: 100 μs, current: 0.8 mA, stimulation: 5 min, suspension: 5 min, repetition: 3 times). The neurological function was evaluated by Beam-Balance test and walking test 1, 3, 7, 14, 21, and 28 d after TBI; Morris Water Maze test was performed to observe the abilities of spatial learning and memory 24-28 d after TBI; the brain tissue sections were obtained for analyzing the volume of cerebral injury 28 d after TBI. Fourteen d after TBI, Nissel staining was used to observe the neuronal morphology and survival cell number of brain injured areas in each group, immunohistochemical staining was employed to detect the number of neuronalnuclear antigen (NeuN) positive neurons in the hippocampal dentate gyrus and CA3 area, and ELISA was used to detect the expressions of interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)-α and nuclear factor (NF)-κB. Western blotting was used to detect the α7 nAChR protein expression levels 3, 7, 14 d after TBI.n Results:As compared with the TBI group, the VNS group showed statistically longer beam-balance latency and shorter beam-walking time 7, 14, 21, and 28 d after TBI, significantly shortened escape latency and prolonged exploration time in the target quadrant 27 and 28 d after TBI (n P<0.05). The volume of cerebral injury in the VNS group was significantly smaller than that in TBI group 28 d after TBI (n P<0.05). As compared with those in the TBI group, the number of Nissel positive neurons around the brain injury area was significantly larger, the number of NeuN positive cells in the hippocampal dentate gyrus and CA3 areas was significantly larger, and the expression levels of IL-1β, IL-6, TNF-α and NF-κB were significantly decreased in the VNS group 14 d after TBI (n P<0.05). The α7 nAChR protein expression in the injury area of VNS group was significantly higher than that of the TBI group 7 and 14 d after TBI (n P<0.05).n Conclusion:VNS treatment can improve the neurobehavioral outcome of TBI rats, which may be linked with the increased α7 nAChR protein expression, and the decreased release of inflammation cytokines IL-1β, IL-6, TNF-α and NF-κB.