RESUMO
OBJECTIVE: This study aimed to investigate the role and mechanism of microRNA (miR)-193a in promoting apoptosis of retinal neuronal cells in early diabetic (DM) rats. METHODS: Seventy-two male SD-grade rats were selected to establish a DM model by intraperitoneal injection of streptozotocin (STZ), and randomly divided into a control group (blank control group), a DM group (diabetic model group), a DM+miR-NC inhibitor group (miR-193a inhibition negative control group), a DM+miR-193a inhibitor group (miR-193a inhibitor group), DM+miR-NC mimic group (miR-193a overexpression negative control group), DM+miR-193a mimic group (miR-193a overexpression group), with12 rats in each group. RESULTS: The miR-193a expression, apoptosis rate, and Bax, Caspase3, and Caspase9 protein expression levels were elevated, and Bcl-2 protein expression was decreased in the retinal tissues of DM rats and high glucose-induced rat retinal neuronal cells, while miR-193a inhibitors reversed these processes. These dual luciferase reporter assay showed that WT1CDS, and WT1Mut were lower in the miR-193a group than in the miR-NC group (P<0.05); WT1 protein expression was reduced in the retinal tissues of DM rat and high glucose-induced rat retinal neuronal cells, and miR-193a inhibitors increased WT1 protein expression. Compared with cells co-transfected with miR-193a and WT1vector, miR-193a and WT1 cotransfection inhibited high glucose-induced apoptosis in retinal neuronal cells and regulated apoptotic protein expression. miR-193a was highly expressed and WT1 was lowly expressed in retinal tissues of DM rats and high glucose-induced rat retinal neuronal cells. CONCLUSION: miR-193a could inhibit early retinal neuronal cell apoptosis in DM rats by targeting and negatively regulating WT1 expression.