目的 比较野生型（WT）小鼠和dysbindin1缺失突变的sdy小鼠睾丸组织来源的外泌体的差异，探讨dysbindin-1在睾丸组织来源的外泌体形成中的可能作用。 方法 1.用蔗糖超速离心法分离WT小鼠和sdy小鼠睾丸组织来源的外泌体，免疫印迹法分析外泌体蛋白的表达，透射电子显微镜负染法观察外泌体的形态，动态光散射粒径分析仪分析颗粒大小分布，质谱分析外泌体的蛋白内容物。2.用磁珠免疫纯化获得CD63+外泌体，进行蛋白组分鉴定，并选取keratin5（krt5）蛋白进行验证。 结果 Dysbindin-1缺失不影响外泌体的形态、数量，但外泌体标记物CD63表达降低。与WT小鼠相比，sdy小鼠睾丸组织的外泌体高表达159种蛋白，低表达209种蛋白，特异性表达184种蛋白。睾丸组织 CD63+外泌体中共筛选到12个蛋白，选取krt5蛋白，显示该蛋白与dysbindin-1有相互作用，并发现dysbindi-1缺失后小鼠睾丸组织来源的外泌体中krt5的表达减少。 结论 Dysbindin-1缺失不影响睾丸组织来源的外泌体的形态和数量，但影响外泌体蛋白的种类和含量，ysbindin-1可能通过蛋白相互作用的方式影响外泌体蛋白的转运。 

Objective To compare the differences in exosomes derived from testicular tissue between WT (wild type) mice and sdy mice with dysbindin-1 (dystrobrevin binding protein 1) deletion mutations, and identify their protein components to explore the possible role of dysbindin-1 in the formation of exosomes derived from mouse testicular tissue.    Methods The exosomes derived from mouse testicular tissue of WT and sdy mice were isolated by sucrose ultracentrifugation method. The expression of exosomes proteins was analyzed by Western blotting, the morphology of exosomes was observed by negative staining under transmission electron microscope(TEM), the particle size and distribution were analyzed by dynamic light scattering particle size analyzer, and the protein contents of exosomes were detected by mass spectrometry analysis. CD63+ exosomes were obtained by immunoprecipitation with magnetic beads. Krt5 (keratin5) protein was selected for validation.    Results Dysbindin-1 deletion did not affect the morphology and quantity of exosomes, but decreased the expression of CD63, a marker of exosomes. Compared with the WT mice, there were 159 proteins that were highly expressed, 209 proteins that were lowly expressed, and 184 proteins that were specifically expressed in the exosomes derived from sdy mice testicular tissue. In this experiment, CD63+ exosomes from testicular tissue were obtained and 12 proteins were screened. There was indeed an interaction between krt5 protein and dysbindin-1. Interestingly, it was found that the expression of krt5 in the exosomes derived from sdy mice testicular tissue decreased after dysbindin-1 deletion.    Conclusion After dysbindin-1 deletion, the morphology and quantity of exosomes derived from mouse testicular tissue are not affected, but dysbindin-1 may affect the types and content of exosomal proteins, by affecting the transport of exosome proteins through protein interactions.