中国口腔颌面外科杂志

中国口腔颌面外科杂志 ›› 2021, Vol. 19 ›› Issue (4): 320-324.doi: 10.19438/j.cjoms.2021.04.006

• 论著 • 上一篇    下一篇

甲状腺激素对小鼠面神经损伤轴突再生及神经电生理功能的影响

陈邢玉1, 董非斐1, 李凯2   

  1. 1.三亚市人民医院 内分泌科,海南 三亚 572000;
    2.杭州艾维口腔门诊部有限公司 金沙大道口腔门诊部,浙江 杭州 310018
  • 收稿日期:2020-11-24 修回日期:2021-01-07 出版日期:2021-07-20 发布日期:2021-08-05
  • 通讯作者: 陈邢玉, E-mail：shellyya5535@163.com
  • 作者简介:陈邢玉 (1984-),女,硕士,主治医师

Effects of thyroid hormone on axon regeneration and electrophysiological function of facial nerve injury in mice

CHEN Xing-yu1, DONG Fei-fei1, LI Kai2   

  1. 1. Department of Endocrinology, The People's Hospital of Sanya. Sanya 572000, Hainan Province;
    2. Jingsha Road Branch, Hangzhou Ivy Dental Clinic Corporation. Hangzhou 310018, Zhejiang Province, China
  • Received:2020-11-24 Revised:2021-01-07 Online:2021-07-20 Published:2021-08-05

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摘要： 目的： 探讨甲状腺激素对小鼠面神经损伤轴突再生及神经电生理功能的影响。方法： 将64只小鼠随机分为4组,即假手术组、模型组、甲状腺素组、甲状腺素+LY组,每组16只。除假手术组外,其余组均建立面神经损伤模型。术后苏醒开始干预,甲状腺素组于损伤处皮下注射50 μg/kg中性甲状腺素溶液,甲状腺素+LY组在甲状腺素组基础上腹腔注射600 μg/kg PI3K/AKT通路抑制剂LY294002,假手术组和模型组于损伤处注射生理盐水,每天1次,持续2周。干预结束后进行神经电生理检测,锇酸染色进行再生轴突计数,Western免疫印迹法检测面神经组织中p-AKT、NGF、BDNF蛋白的表达。采用SPSS 21.0软件包对数据进行统计学分析。结果： 假手术组正常神经髓鞘外未见新生轴突。与模型组相比,甲状腺素组和甲状腺素+LY组再生轴突数均升高,甲状腺素组显著高于甲状腺素+LY组（P<0.05）。与假手术组相比,模型组运动神经传导速度（MNCV）和波幅降低,潜伏期延长（P<0.05）;与模型组相比,甲状腺素组和甲状腺素+LY组MNCV、波幅升高,甲状腺素组显著高于甲状腺素+LY组（P<0.05）;与模型组相比,甲状腺素组和甲状腺素+LY组潜伏期缩短,甲状腺素组显著短于甲状腺素+LY组（P<0.05）。与假手术组相比,模型组p-AKT、NGF、BDNF蛋白相对表达量显著升高（P<0.05）;与模型组相比,甲状腺素组p-AKT蛋白相对表达量显著升高,甲状腺素+LY组显著降低（P<0.05）;与模型组相比,甲状腺素组和甲状腺素+LY组NGF、BDNF蛋白相对表达量升高,甲状腺素组显著高于甲状腺素+LY组（P<0.05）。结论： 甲状腺激素可有效促进小鼠面神经损伤轴突再生,改善神经电生理功能,其机制可能是通过促进AKT磷酸化而发挥调控作用。

关键词: 面神经损伤, 甲状腺激素, 轴突再生, 神经电生理

Abstract: PURPOSE: To investigate the effect of thyroid hormone on axon regeneration and neurophysiological function of facial nerve injury in mice. METHODS: Sixty-four mice were randomly divided into 4 groups: sham operation group, model group, thyroxine group, and thyroxine + LY group, each with 16 mice. Except for the sham operation group, facial nerve injury models were established in the remaining groups. Intervention was started after recovery: the thyroxine group was injected subcutaneously with 50 μg/kg neutral thyroxine solution, the thyroxine + LY group was intraperitoneally injected with 600 μg/kg PI3K/AKT pathway inhibitor LY294002 on the basis of the thyroxine group. The sham operation group and model group were injected with normal saline once a day for 2 weeks. After intervention, neuroelectrophysiological test was performed, the number of regenerated axons were counted by osmium acid staining, and the expression of p-AKT, NGF and BDNF protein in facial nerve tissue was detected by Western blot. SPSS 21.0 software package was used for data analysis. RESULTS: In the sham operation group, no new axons were found outside the myelin sheath of normal nerves. Compared with the model group, the number of regenerated axons in the thyroxine group and the thyroxine + LY group both increased, and the thyroxine group was significantly higher than the thyroxine + LY group(P<0.05). Compared with the sham operation group, the motor nerve conduction velocity (MNCV) and amplitude of the model group were reduced, and the incubation period was prolonged(P<0.05). Compared with the model group, the MNCV and amplitude of the thyroxine group and the thyroxine + LY group were increased, and the thyroxine group was significantly higher than that of the thyroxine + LY group(P<0.05). Compared with the model group, the latency of the thyroxine group and the thyroxine + LY group were shortened, and the thyroxine group was significantly shorter than the thyroxine + LY group (P<0.05). Compared with the sham operation group, the relative expression of p-AKT, NGF and BDNF protein in the model group significantly increased(P<0.05). Compared with the model group, the relative expression of p-AKT protein in the thyroxine group increased, while that in the thyroxine+LY group significantly decreased(P<0.05). Compared with the model group, the relative expression of NGF and BDNF protein in the thyroxine group and the thyroxine + LY group increased, and the thyroxine group was significantly higher than thyroxine + LY group (P<0.05). CONCLUSIONS: Thyroid hormone can effectively promote the regeneration of facial nerve axons in mice and improve the electrophysiological function of the nerve. Its mechanism may be through promoting the activation of AKT phosphorylation and play a regulatory role.

Key words: Facial nerve injury, Thyroid hormone, Axon regeneration, Neuroelectrophysiology

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