TY - JOUR AB - Injury to terminally differentiated podocytes contributes ignificantly to proteinuria and glomerulosclerosis. The aim of this study was to examine the protective effects of notoginsenoside R1 (NR1) on the maintenance of podocyte number and foot process architecture via the inhibition of apoptosis, the induction of autophagy and the maintenance pf podocyte biology in target cells. The effects of NR1 on conditionally immortalized human podocytes under high glucose conditions were evaluated by determining the percentage apoptosis, the percentage autophagy and the expression levels of slit diaphragm proteins. Our results revealed that NR1 protected the podocytes against high glucose-induced injury by decreasing apoptosis, increasing autophagy and by promoting cytoskeletal recovery. The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway was further investigated in order to elucidate the mechanisms responsible for the protective effects of NR1 on podocytes. Our data indicated that treatment with NR increased the phosphorylation levels of PI3K, Akt and mTOR, leading to the activation of the PI3K/Akt/mTOR signaling pathway in podocytes. To the best of our knowledge, this is the first in vitro study to demonstrate that NR1 protects podocytes by activating the PI3K/Akt/mTOR pathway. AD - Department of Nephrology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China Department of Gynecology, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, P.R. China School of Basic Medical Science, Guangxi University of Chinese Medicine, Nanning, Guangxi 530001, P.R. China Department of Biomedical Engineering, Medical School of University of Electronic Science and Technology of China, Chengdu, Sichuan 610054, P.R. China Center for Perinatal Research, Research Institute at Nationwide Children's Hospital, Columbus, OH 43215, USA AU - Huang,Guodong AU - Zou,Bingyu AU - Lv,Jianzhen AU - Li,Tongyu AU - Huai,Guoli AU - Xiang,Shaowei AU - Lu,Shilong AU - Luo,Huan AU - Zhang,Yaping AU - Jin,Yi AU - Wang,Yi DA - 2017/03/01 DO - 10.3892/ijmm.2017.2864 EP - 568 IS - 3 JO - Int J Mol Med KW - podocyte apoptosis autophagy notoginsenoside R1 PI3K/Akt/mTOR pathway PY - 2017 SN - 1107-3756 1791-244X SP - 559 ST - Notoginsenoside R1 attenuates glucose-induced podocyte injury via the inhibition of apoptosis and the activation of autophagy through the PI3K/Akt/mTOR signaling pathway T2 - International Journal of Molecular Medicine TI - Notoginsenoside R1 attenuates glucose-induced podocyte injury via the inhibition of apoptosis and the activation of autophagy through the PI3K/Akt/mTOR signaling pathway UR - https://doi.org/10.3892/ijmm.2017.2864 VL - 39 ER -