摘要●目的:研究自噬抑制剂3-甲基趋化(3-MA)在糖尿病小鼠模型(DM)和潜在机制上的作用。●方法:将雄性C57BL/6J小鼠随机分为正常对照组(NC组)和DM组。dm是通过多种低剂量腹膜内注射链蛋白酶(STZ)60 mg/kg●连续5天诱导的。dm小鼠随机细分为未处理的组(DM组),3-ma(10 mg/kg●dm gavage)治疗组(DM+3-ma组)和氯喹(CQ; 50 mg/kg通过腹膜内注射)治疗组(DM+CQ组)。每周记录空腹血糖(FBG)水平。在实验结束时,收集了视网膜样品。The expression levels of pro-apoptotic proteins cleaved caspase-3, cleaved poly ADP-ribose polymerase 1 (PARP1) and Bax, anti-apoptotic protein Bcl-2, fibrosis- associated proteins Fibronectin and type 1 collagen α1 chain (COL1A1), vascular endothelial growth factor (VEGF), inflammatory factors interleukin (IL)-1β和肿瘤坏死因子(TNF)-α以及自噬相关蛋白LC3,