China Journal of Oral and Maxillofacial Surgery ›› 2021, Vol. 19 ›› Issue (4): 320-324.doi: 10.19438/j.cjoms.2021.04.006

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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

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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