Rosiglitazone (RSG) is widely used to reduce the amount of sugar in the blood of patients with diabetes mellitus. Diabetic nephropathy is the most common microvascular complication of diabetes. The role of RSG in diabetic nephropathy is not fully understood. Diabetic nephropathy model was constructed in high glucose (HG)-treated mouse mesangial cells. The effects of RSG on cell viability and cell cycle were investigated using cell counting kit-8 (CCK-8) assay and flow cytometry assay. Oxidative stress was assessed according to ROS production and SOD activity in cells. Inflammatory responses were assessed according to the releases of inflammatory cytokines. Extracellular matrix (ECM) accumulation was determined by the levels of fibronectin and collagen IV using western blot. The expression of Gm26917 and microRNA-185-5p (miR-185-5p) was detected by quantitative real-time polymerase chain reaction (qPCR). The interaction between Gm26917 and miR-185-5p was validated by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and pull-down assay. RSG significantly inhibited HG-induced proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells. The expression of Gm26917 was induced by HG but weakened by RSG. Gm26917 knockdown alleviated HG-induced proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells, and Gm26917 overexpression partly abolished the effects of RSG. Moreover, miR-185-5p was a target of Gm26917, and miR-185-5p inhibition recovered proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells that were alleviated by Gm26917 knockdown. RSG ameliorated HG-induced mouse mesangial cell proliferation, oxidative stress, inflammation and ECM accumulation partially by governing the Gm26917/miR-185-5p pathway.

罗格列酮 (RSG) 广泛用于降低糖尿病患者血液中的糖含量。糖尿病肾病是糖尿病最常见的微血管并发症。RSG 在糖尿病肾病中的作用尚不完全清楚。在高糖（HG）处理的小鼠系膜细胞中构建糖尿病肾病模型。使用细胞计数试剂盒 8 (CCK-8) 测定和流式细胞术测定研究 RSG 对细胞活力和细胞周期的影响。根据细胞中的 ROS 产生和 SOD 活性评估氧化应激。根据炎症细胞因子的释放评估炎症反应。使用蛋白质印迹通过纤连蛋白和胶原蛋白 IV 的水平确定细胞外基质 (ECM) 的积累。通过定量实时聚合酶链反应（qPCR）检测Gm26917和microRNA-185-5p（miR-185-5p）的表达。Gm26917 和 miR-185-5p 之间的相互作用通过双荧光素酶报告基因测定、RNA 免疫沉淀 (RIP) 测定和下拉测定进行验证。RSG 显着抑制 HG 诱导的小鼠系膜细胞增殖、氧化应激、炎症反应和 ECM 积累。Gm26917的表达被HG诱导，但被RSG减弱。Gm26917 敲低减轻了 HG 诱导的小鼠系膜细胞增殖、氧化应激、炎症反应和 ECM 积累，而 Gm26917 过表达部分消除了 RSG 的作用。此外，miR-185-5p 是 Gm26917 的靶标，抑制 miR-185-5p 可恢复增殖、氧化应激、Gm26917 敲低可减轻小鼠系膜细胞中的炎症反应和 ECM 积累。RSG 通过调控 Gm26917/miR-185-5p 通路部分改善了 HG 诱导的小鼠系膜细胞增殖、氧化应激、炎症和 ECM 积累。