目的：探讨大鼠面神经损伤失神经支配2个月后，面肌（鼻唇提肌）的形态学变化及收缩相关蛋白α-肌 动蛋白与α-辅肌动蛋白的表达差异，以阐明失神经后面肌萎缩与功能减退的病理机制。方法：健康成年SD 大鼠20只，左侧切断面神经出茎乳孔处主干建立失神经支配模型（断伤侧），右侧作相同切口仅暴露面神经 （对照侧）。术后2个月，取双侧鼻唇提肌，进行湿重测量、Masson染色观察肌细胞形态与胶原纤维增生情 况，并采用免疫组织化学染色检测α-肌动蛋白与α-辅肌动蛋白的表达水平。结果：断伤侧鼻唇提肌湿重显 著低于对照侧（P＜0.05）。Masson染色显示断伤侧肌细胞数量减少、直径与横截面积减小，胶原纤维占比显 著增高（均P＜0.05）。免疫组化结果显示，断伤侧α-肌动蛋白表达显著下降（P＜0.05），而α-辅肌动蛋白表达 2组间差异无统计学意义（P＞0.05）。结论：大鼠面神经切断2个月后，面肌出现明显萎缩、胶原纤维增生及 收缩蛋白α-肌动蛋白表达降低，提示失神经支配导致面肌结构退化与收缩功能减弱。后续研究需进一步分 阶段观察并优化实验方法，以深入揭示其机制并探索修复策略。

To investigate the morphological changes in the facial muscle (specifically, the levator nasolabial muscle) and differences in the expression of contraction-related proteins α-actin and α-actinin following two months of denervation due to facial nerve injury in rats, aiming to elucidate the pathological mechanisms underlying facial muscle atrophy and functional decline post-denervation. Methods: Twenty healthy adult Sprague-Dawley (SD) rats were used. A model of denervation was established by transecting the main trunk of the left facial nerve at its exit from the stylomastoid foramen, while on the right side, only exposure of the facial nerve via an identical surgical approach served as the control. Two months after surgery, bilateral levator nasolabial muscles were harvested for analysis. Wet weights were measured, Masson's trichrome staining was performed to assess myofiber morphology and collagen fiber proliferation, and immunohistochemical staining was employed to detect the expression levels of α-actin and α-actinin. Results: The wet weight of the denervated (lesioned) side was significantly lower than that of the control side (P<0.05). Masson's staining revealed reduced number, diameter, and cross-sectional area of myofibers, along with significantly increased collagen deposition on the lesioned side (all P<0.05). Immunohistochemistry showed a marked decrease in α-actin expression on the denervated side (P<0.05), whereas no statistically significant difference in α-actinin expression was observed between the two sides (P>0.05). Conclusion: After two months of facial nerve transection, rats exhibited obvious facial muscle atrophy, enhanced collagen fibrosis, and downregulated expression of the contractile protein α-actin, indicating structural degeneration and impaired contractile function induced by denervation. Future studies should conduct staged observations and refine experimental methodologies to further uncover the underlying mechanisms and explore potential therapeutic strategies.