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Oleanolic acid attenuated diabetic mesangial cell injury by activation of autophagy via miRNA-142-5p/PTEN signaling

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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… Click to show full abstract

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.

Keywords: nrk 52e; mir 142; autophagy; 52e cells; oleanolic acid; 142 pten

Journal Title: Cytotechnology
Year Published: 2019

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