【摘要】 目的建立I型疱疹病毒感染致小鼠面神经麻痹的动物模型,并探讨单纯疱疹病毒1型(herpes simplex virus type1,HSV-1)在小鼠面神经麻痹发生过程中的致病机制及作用部位。方法选择53只16~18g、4周龄雌性Balb/c小鼠,用26G针头在49只实验组小鼠右耳廓背面近耳根部皮肤连续搔刮后,将25μL HSV-1病毒液滴在创面上。同样方法搔刮左耳廓,滴25μL PBS作为对照。另4只动物不作处理,作为空白对照。PCR法检测接种病毒后不同时间段的实验动物相关部位的HSV-1DNA表达。结果49只接种动物中,37只(75.51%)出现不同程度的面神经麻痹。其中,右侧14只(14/37,37.84%),左侧3只(8.11%),双侧20只(54.05%)。20只双侧面神经麻痹动物中,13只(65%)先出现右侧面神经麻痹,2只(10%)先出现左侧面神经麻痹,另外5只直接发生双侧面神经麻痹。37只面神经麻痹动物中,6只(16.22%)面神经麻痹自行恢复,平均恢复时间为7.83d。结论HSV-1存在于脑干和大脑皮层面神经运动核放射区与面神经麻痹的出现关系密切。更多还原

【Abstract】 Objective To establish an animal model of Bell palsy induced by type I herpes simplex virus (HSV-1) infection and to assess the role and site of HSV-1 in the pathogenesis of facial paralysis. Methods Fifty-three female Balb/c mice four-week-old weighted 16-18 g were studied. After scratching the surface of bilateral auricles with a 26-gauge needle, 25μL HSV-1 with a titer of 6.7×107 PFU/ml was inoculated into the right auricle, and the same volume of PBS was placed in the left. As a control, PBS was placed on the bilateral auricles of 4 mice. The HSV-1 DNA in bilateral facial nerve, bilateral brainstem, bilateral trigeminal carrierl ganglion, bilateral brain, and blood at different stage was examined with polmerase chain reaction analysis. Results Thirty-seven animals (75.51%) appeared different degree facial paralysis among the 49 inoculated animals. Fourteen facial paralysis (37.84%) were on the right, 3 (8.11%) on the left, and 20 (54.05%) on the bilateral side. Six animals with facial palsy were recovered during 3-13 days, the average recovery time was 7.83 days. Conclusions The existence of HSV-1 in the brainstem and the cerebral cortex is significant for facial paralysis.更多还原