Ginsenoside Rg1 reduces aldosterone-induced autophagy via the AMPK/mTOR pathway in NRK-52E cells

Wang,Li; Mao,Nan; Tan,Rui‑Zhi; Wang,Hong‑Lian; Wen,Ji; Liu,Yu‑Hang; Furhad,Md; Fan,Jun‑Ming

doi:10.3892/ijmm.2015.2242

Ginsenoside Rg1 reduces aldosterone-induced autophagy via the AMPK/mTOR pathway in NRK-52E cells

Authors:
- Li Wang
- Nan Mao
- Rui‑Zhi Tan
- Hong‑Lian Wang
- Ji Wen
- Yu‑Hang Liu
- Md Furhad
- Jun‑Ming Fan
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Affiliations: State Key Laboratory of Biotherapy of Human Disease, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China, Department of Nephrology, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610000, P.R. China, Research Center of Combine Traditional Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Luzhou Medical College, Luzhou, Sichuan 646000, P.R. China, Department of Immunology and Rheumatology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China, Department of Nephrology, The Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan 646000, P.R. China
Published online on: June 10, 2015 https://doi.org/10.3892/ijmm.2015.2242
Pages: 518-526

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Abstract

Aldosterone is a steroid hormone secreted from the adrenal cortex, which regulates blood pressure. Higher concentrations of aldosterone can cause several diseases, including hypertension, diabetic nephropathy and chronic kidney disease. Previous reports have demonstrated that aldosterone has a pathogenic role in renal injury via reactive oxygen species (ROS), which involves the regulation of autophagy. However, whether aldosterone can induce autophagy in renal tubular cells remains to be elucidated. In the present study, elevated autophagy was observed in rat renal tubular NRK‑52E cells exposed to aldosterone, which was demonstrated by the increased number of autophagosomes, conversion of LC3‑I to LC3‑II and the expression of Beclin‑1. The enhanced autophagy was accompanied by increased production of intracellular ROS, which was reversed by N‑acetylcysteine, a specific inhibitor of ROS signaling. Furthermore, treatment with ginsenoside Rg1 reduced the aldosterone‑induced autophagy and production of ROS, possibly through reducing the phosphorylation of AMPK and preserving mTOR activity. These findings demonstrated that aldosterone promoted ROS generation and increased autophagy in the NRK‑52E cells. Ginsenoside Rg1 effectively relieved aldosterone‑induced oxidative stress and abnormal autophagy, suggesting that Rg1 may be used as a potential therapeutic drug to inhibit the renal injury, which is induced by aldosterone.

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