神经肌肉损伤是压力性尿失禁（SUI）的主要病因。目前干细胞尿道括约肌注射主要针对尿道括约肌的恢复，缺乏对神经的修复，且干细胞治疗，存在染色体变异，致癌性，免疫排斥反应和伦理限制等问题。我们将ADSCs体外诱导为神经样细胞，并提取外泌体，体外研究发现ADSCs来源的神经样细胞外泌体可以促进成肌细胞生长，同时可以促进施旺细胞增殖、迁移和修复表型转化，而施旺细胞c-JUN/JNK信号通路激活可能在ADSCs来源的神经样细胞外泌体修复压力性尿失禁神经损伤中发挥重要作用。本课题，我们提取ADSCs来源的神经样细胞外泌体，在体外和SUI动物模型验证肌肉、神经修复的作用，并进一步采用细胞因子芯片及基因表达谱高通量测序等技术明确ADSCs来源的神经样细胞外泌体激活施旺细胞c-JUN/JNK信号通路对神经修复的分子机制，为该项技术向临床治疗转化，提供前期实验基础。

Neuromuscular damage is the major cause of the stress urinary incontinence (SUI). Urethral injection of stem cells focuses on restoring sphincteric function, while little aims to restore neurogenic etiologies. Meanwhile, the direct use of stem cells remains restricted by issues such as potential chromosomal variation, tumorigenicity, immunological rejection, and ethical limitations. We obtained neuro-induced ADSCs from ADSCs, and extracted the exosomes. we found the exosomes neuro-induced ADSCs not only can promote the growth of smooth muscle cells, but also enhance the proliferation, migration, repair phenotypic transformation of Schwann Cell. The activation of c-JUN/JNK signal pathway in Schwann Cell may play a critical role in the restoration of the nerve defect. In this study, we obtained the exosomes from neuro-induced ADSCs, and analyze the effect of exosomes on the regeneration of the smooth muscle and neuron in vitro and SUI rat models. We further clear the molecular mechanism of exosomes from neuro-induced ADSCs activation of c-JUN/JNK signal pathway in Schwann Cell using PCR array and sequence test and provide the pre-clinical for the clinical treatment conversion.