T细胞免疫缺陷小鼠创伤性面瘫模型的建立及其形态学评价

目的 尝试建立T细胞免疫缺陷小鼠面瘫模型，并运用形态学技术分析免疫缺陷小鼠的面神经损伤特点，深入探讨面神经修复再生的神经免疫病理机制提供实验基础。方法 切断裸鼠面神经出茎乳孔主干，于术后2周灌注固定动物，收集脑干切片，荧光金逆行示踪技术标记面运动神经元损伤情况，并结合面神经周围主干锇酸染色情况分析裸鼠面神经损伤特点。结果 术后观察免疫缺陷小鼠面瘫出现情况,如瞬目反射、触须拂动、鼻尖方向、耳廓运动等均出现典型的完全周围性面瘫，术后14d裸鼠右侧面神经损伤远端锇酸染色显示面神经重度变性。面瘫小鼠面神经核团可见“健康”、“受损”、“死亡”的各型面运动神经元。T细胞免疫缺陷小鼠与野生型小鼠面神经核团计数有显著性差异。结论 T细胞免疫缺陷的小鼠创伤性面瘫模型稳定、可行，为进一步深入揭示外伤性面瘫发生与演进过程中以T细胞行为研究为中心的神经免疫病理机制提供了实验基础。

Establishment and morphological assessment of the T-cell immune deficiency mouse model with facial nerve axotomy

Objective To establish a stable and reliable T-cell immune deficiency mouse model with facial nerve axotomy by the application and assessment with morphological methodson the immune deficiency mouse with facial nerve transection, so as to provide an experimental foundation for revealing the latent neuroimmunological mechanism of traumatic facial paralysis. Methods The T-cell deficiency mice were subjected to a right facial nerve axotomy. Fluorogold retrotracer was used at a designated time. Two weeks after the operation, the slices of the brain stem were collected and the facial moto-neurons were observed and counted. Also, the injured facial nerve of axotomy nude mice was assessed with osmic acid staining. Results All the mice presented typical facial paralysis after the transection of the facial nerve. Remarkable degenerations were observed in the distal end of the transected facial nerve on the 14th day after the operation. There was different status among the motoneurons in the facial nuclus, such as healthful, injured or dead. Significant difference in the number of facial moto-neurons between the nude mouse group and the wild type mouse group was noticed. Conclusion The T-cell immune deficiency mouse model with facial nerve axotomy is effectiveand feasible. It provides an experimental foundation for revealing the latent neuroimmunological mechanism centering on T cell behavior of the pathogenesis and progression of facial nerve trauma.