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

doi:10.19438/j.cjoms.2021.04.006

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

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

1.三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. 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

摘要/Abstract

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

中图分类号:

R741

陈邢玉, 董非斐, 李凯. 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[J]. 中国口腔颌面外科杂志, 2021, 19(4): 320-324.

CHEN Xing-yu, DONG Fei-fei, LI Kai. Effects of thyroid hormone on axon regeneration and electrophysiological function of facial nerve injury in mice[J]. China J Oral Maxillofac Surg, 2021, 19(4): 320-324.

参考文献

[1] Condie D, Tolkachjov SN.Facial nerve injury and repair: a practical review for cutaneous surgery[J]. Dermatol Surg, 2019, 45(3): 340-357.
[2] Ma F, Zhu T, Xu F, et al.Neural stem/progenitor cells on collagen with anchored basic fibroblast growth factor as potential natural nerve conduits for facial nerve regeneration[J]. Acta Biomater, 2017, 50: 188-197.
[3] Liu YC, Yeh CT, Lin KH.Molecular functions of thyroid hormone signaling in regulation of cancer progression and anti-apoptosis[J]. Int J Mol Sci, 2019, 20(20):4986-5013.
[4] 张秋兰, 樊艳婷, 李琳, 等. 促甲状腺激素水平与2型糖尿病患者周围神经病变的相关性[J]. 中国医药, 2018, 13(11): 1686-1690.
[5] Lee EH, Kim SM, Kim CH, et al.Dopamine neuron induction and the neuroprotective effects of thyroid hormone derivatives[J]. Sci Rep, 2019, 9(1):13659.
[6] 张风河, 黄萍, 杨丕山, 等. p75神经营养蛋白受体基因敲除对小鼠面神经损伤后神经再生的影响[J]. 华西口腔医学杂志, 2010, 28(1): 95-98.
[7] Canale ST, Beaty JH.坎贝尔骨科手术学.周围神经损伤与显微外科分册[M]. 天津: 天津科技翻译出版公司, 2013:93-94.
[8] Takezawa K, Townsend G, Ghabriel M.The facial nerve: anatomy and associated disorders for oral health professionals[J]. Odontology, 2018, 106(2):103-116.
[9] Moin A, Shetty AD, Archana TS, et al.Facial nerve injury in temporomandibular joint approaches[J]. Ann Maxillofac Surg, 2018, 8(1): 51-55.
[10] Gao D, Tang T, Zhu J, et al.CXCL12 has therapeutic value in facial nerve injury and promotes Schwann cells autophagy and migration via PI3K-AKT-mTOR signal pathway[J]. Int J Biol Macromol, 2019, 124: 460-468.
[11] Wu L, Han D, Jiang J, et al.Co-transplantation of bone marrow mesenchymal stem cells and monocytes in the brain stem to repair the facial nerve axotomy[J]. Eur J Histochem, 2020, 64(s2):3136-3148.
[12] Salazar P, Cisternas P, Martinez M, et al.Hypothyroidism and cognitive disorders during development and adulthood: implications in the central nervous system[J]. Mol Neurobiol, 2019, 56(4):2952-2963.
[13] 韦春珠, 王学敏, 潘宇政. 外源性甲状腺素对重型创伤性脑损伤大鼠中枢神经再生修复的作用[J]. 中华创伤杂志, 2019, 35(5): 400-406.
[14] Wei C, Luo Y, Peng L, et al.Expression of Notch and Wnt/β-catenin signaling pathway in acute phase severe brain injury rats and the effect of exogenous thyroxine on those pathways[J]. Eur J Trauma Emerg Surg, 2020, 46(3): 316-326.
[15] Satish A, Korrapati PS.Strategic design of peptide-decorated aligned nanofibers impregnated with triiodothyronine for neural regeneration[J]. J Tissue Eng Regen Med, 2019, 13(5): 753-770.
[16] Jia H, Wang Y, Chen J, et al.Combination of BMSCs-laden acellular nerve xenografts transplantation and G-CSF administration promotes sciatic nerve regeneration[J]. Synapse, 2019, 73(7):e22093.
[17] Huang HT, Sun ZG, Liu HW, et al.ERK/MAPK and PI3K/AKT signal channels simultaneously activated in nerve cell and axon after facial nerve injury[J]. Saudi J Biol Sci, 2017, 24(8): 1853-1858.
[18] Tian Z, Tang C, Wang Z.Neuroprotective effect of ginkgetin in experimental cerebral ischemia/reperfusion via apoptosis inhibition and PI3K/Akt/mTOR signaling pathway activation[J]. J Cell Biochem, 2019, 120(10):18487-18495.
[19] Zhang YP, Liu SY, Sun QY, et al.Proanthocyanidin B2 attenuates high-glucose-induced neurotoxicity of dorsal root ganglion neurons through the PI3K/Akt signaling pathway[J]. Neural Regen Res, 2018, 13(9):1628-1636.

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

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

PDF (PC)

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 1

编辑推荐

Metrics

本文评价