To investigate the expression level of miR-25-3p in patients with type 2 diabetes mellitus (T2DM) and diabetic nephropathy (DN), and its effect on proliferation, apoptosis and inflammatory response of mesangial cells cultured with high glucose. Blood samples of all clinical subjects were collected for RT-qPCR analysis to detect serum miR-25-3p levels. Human mesangial cells (HMCs) cultured with high glucose were used to construct DN model in vitro. MTT assay, flow cytometry and ELISA were used to evaluate the effects of miR-25-3p on the proliferation, apoptosis, and inflammatory response of DN cell models. Serum miR-25-3p was decreased in both T2DM group and DN group, but more in DN group. Serum miR-25-3p was positively correlated with eGFR and negatively correlated with UAER. The expression of miR-25-3p was reduced in HMCs induced by high glucose. Transfection of miR-25-3p mimic could significantly up-regulate the miR-25-3p level in HMCs. Besides, high glucose culture resulted in abnormal proliferation of HMCs, reduced apoptotic cells, and increased inflammation. The addition of miR-25-3p mimic significantly inhibited cell proliferation and promoted cell apoptosis and reduced the production of inflammatory factors. The abnormal reduction of serum miR-25-3p in DN indicates that it may be a potential biomarker for clinical diagnosis of DN. In in vitro experiments, miR-25-3p was involved in the progression of DN by regulating cell proliferation, apoptosis, and inflammatory response.

探讨miR-25-3p在2型糖尿病（T2DM）和糖尿病肾病（DN）患者中的表达水平及其对高糖培养的系膜细胞增殖、凋亡和炎症反应的影响。收集所有临床受试者的血样进行RT-qPCR分析以检测血清miR-25-3p水平。采用高糖培养的人系膜细胞（HMC）构建体外DN模型。采用MTT法、流式细胞术和ELISA法评价miR-25-3p对DN细胞模型增殖、凋亡和炎症反应的影响。 T2DM组和DN组血清miR-25-3p均下降，但DN组下降较多。血清miR-25-3p与eGFR呈正相关，与UAER呈负相关。高糖诱导的 HMC 中 miR-25-3p 的表达降低。转染 miR-25-3p 模拟物可以显着上调 HMC 中 miR-25-3p 的水平。此外，高糖培养导致HMCs异常增殖、凋亡细胞减少、炎症增加。添加miR-25-3p模拟物显着抑制细胞增殖并促进细胞凋亡并减少炎症因子的产生。 DN 中血清 miR-25-3p 的异常降低提示其可能成为 DN 临床诊断的潜在生物标志物。在体外实验中，miR-25-3p通过调节细胞增殖、凋亡和炎症反应参与DN的进展。