Oleanolic acid (OA), a potential drug for diabetic nephropathy (DN) treatment was found to downregulate the expression of microRNA (miR). The research aimed to investigate the effect of OA on autophagy mediated through miR-142-5p targeted PTEN signal. NRK-52E cells were cultured under normal or high glucose condition. DN model were induced by intravenous injection with streptozotocin (55 mg/kg). Renal fibrosis mice were detected by hematoxylin and eosin (HE) staining, Masson staining and immunohistochemistry assay. TargetScan and dual-luciferase reporter assay system was used to detect the target of miR-142-5p. Expression levels of microRNA and proteins were analyzed by real-time PCR and western blotting. Autophagy was decreased in the progression of renal fibrosis in diabetic nephropathy mice (in vivo) and in high glucose-induced NRK-52E cells (rat kidney epithelial cells) (in vitro) as the expression ofLC-3I and LC-3II (indicators of autophagy) were decreased mice MiR-142-5p was unregulated and PTEN was down-regulated in kidney mice and high glucose-induced NRK-52E cells. Targetscan prediction revealed that PTEN was a target of miR-142-5p. OA restricted HG-induced NRK-52E cell fibrosis through inhibition of miR-142-5p to promote PTEN expression and autophagy levels. To sum up, the research indicated that OA promoted autophagy through inhibition of PI3K/AKT/mTOR pathway. OA alleviated diabetic renal fibrosis by increasing autophagy through regulation of miR-142-5p/PTEN via PI3K/AKT/mTOR pathway in NRK-52E cells.

中文翻译：

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齐墩果酸通过经由miRNA-142-5p / PTEN信号传导的自噬激活来减轻糖尿病系膜细胞损伤。

发现齐墩果酸（OA）是糖尿病性肾病（DN）治疗的潜在药物，下调microRNA（miR）的表达。该研究旨在研究O​​A对通过miR-142-5p靶向的PTEN信号介导的自噬的影响。在正常或高葡萄糖条件下培养NRK-52E细胞。通过静脉内注射链脲佐菌素（55 mg / kg）诱导DN模型。用苏木精和曙红（HE）染色，Masson染色和免疫组化法检测肾纤维化小鼠。使用TargetScan和双荧光素酶报告基因检测系统检测miR-142-5p的靶标。通过实时PCR和蛋白质印迹分析microRNA和蛋白质的表达水平。随着LC-3I和LC-3II的表达（糖尿病的指标），糖尿病肾病小鼠（体内）和高糖诱导的NRK-52E细胞（大鼠肾上皮细胞）（体外）的肾纤维化进程自噬降低。自体吞噬）降低的小鼠在肾小鼠和高糖诱导的NRK-52E细胞中，MiR-142-5p不受调控，而PTEN被下调。Targetscan预测显示PTEN是miR-142-5p的靶标。OA通过抑制miR-142-5p促进PTEN表达和自噬水平来限制HG诱导的NRK-52E细胞纤维化。综上所述，研究表明OA通过抑制PI3K / AKT / mTOR途径促进自噬。OA通过通过PI3K / AKT / mTOR通路调节miR-142-5p / PTEN来调节NRK-52E细胞中的自噬，从而减轻糖尿病性肾纤维化。