Diabetic nephropathy (DN) seriously threatens the health of patients with diabetes. Moreover, it has been reported that mesenchymal stem cell (MSC)-derived exosomal miRNAs can modulate the progression of multiple diseases, including DN. It has been suggested that miR-125b is involved in DN. However, the biological functions of exosomal miRNAs, especially miR-125b, in DN are still unclear. To establish a DN model in vitro, we used a model of human embryonic kidney epithelial cells (HKCs) injury induced by high glucose (HG). Then, miR-125b was delivered to the model cells in vitro via MSC-derived exosomes (MSC-Exos), and the effect of exosomal miR-125b on HKCs apoptosis was evaluated by flow cytometry. qRT-PCR or western blotting was performed to measure miR-125b or tumour necrosis factor receptor-associated factor 6 (TRAF6) expression in HKC. The effect of MSC-Exos on HKCs apoptosis after miR-125b knockdown was determined by flow cytometry. Moreover, dual-luciferase reporter assays were used to determine the targeting relationship between miR-125b and TRAF6 in HKCs. Our data revealed that MSC-Exos increased HG-induced autophagy in HKCs and reversed HKCs apoptosis. Moreover, our study found that miR-125b was enriched in MSC-Exos and directly targeted TRAF6 in HKCs. In addition, exosomally transferred miR-125b inhibited the apoptosis of HG-treated HKCs by mediating Akt signalling. In summary, MSC-derived exosomal miR-125b induced autophagy and inhibited apoptosis in HG-treated HKCs via the downregulation of TRAF6. Therefore, our study provided a new idea for DN treatment.

糖尿病肾病（DN）严重威胁糖尿病患者的健康。此外，据报道，间充质干细胞 (MSC) 衍生的外泌体 miRNA 可以调节包括 DN 在内的多种疾病的进展。有人提出 miR-125b 参与 DN。然而，外泌体 miRNA，尤其是 miR-125b，在 DN 中的生物学功能仍不清楚。为了建立体外DN模型，我们使用了高糖（HG）诱导的人胚胎肾上皮细胞（HKCs）损伤模型。然后，将miR-125b通过体外 递送至模型细胞通过流式细胞术评估MSC衍生的外泌体（MSC-Exos）和外泌体miR-125b对HKCs凋亡的影响。进行 qRT-PCR 或蛋白质印迹以测量 HKC 中 miR-125b 或肿瘤坏死因子受体相关因子 6 (TRAF6) 的表达。通过流式细胞术测定 MSC-Exos 对 miR-125b 敲低后 HKCs 凋亡的影响。此外，双荧光素酶报告基因检测用于确定 miR-125b 和 TRAF6 在 HKCs 中的靶向关系。我们的数据显示，MSC-Exos 增加了 HG 诱导的 HKCs 自噬并逆转了 HKCs 的凋亡。此外，我们的研究发现 miR-125b 富含 MSC-Exos 并直接靶向 HKCs 中的 TRAF6。此外，外泌体转移的 miR-125b 通过介导 Akt 信号传导抑制 HG 处理的 HKCs 的凋亡。总之，通过下调TRAF6。因此，我们的研究为DN治疗提供了新思路。