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Research Paper|Volume 10, Issue 12|pp 4197—4212

Hyperoside attenuates renal aging and injury induced by D-galactose via inhibiting AMPK-ULK1 signaling-mediated autophagy

Buhui Liu1,2, Yue Tu3, Weiming He2, Yinglu Liu1, Wei Wu4, Qijun Fang4, Haitao Tang5, Renmao Tang5, Ziyue Wan6, Wei Sun2, Yigang Wan4
  • 1Department of Traditional Chinese Medicine, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210008, China
  • 2Department of Nephrology, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China
  • 3Department of TCM Health Preservation, Second Clinic Medical School, Nanjing University of Chinese Medicine, Nanjing 210023, China
  • 4Department of Traditional Chinese Medicine, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing 210008, China
  • 5Institute of Huangkui, Suzhong Pharmaceutical Group Co., Ltd., Taizhou 225500, China
  • 6Department of Social Work, Meiji Gakuin University, Tokyo 108-8636, Japan

* * Equal contribution

Received: June 28, 2018Accepted: December 12, 2018Published: December 24, 2018
https://doi.org/10.18632/aging.101723

Copyright: © 2018 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The kidney is a typical organ undergoing age and injury. Hyperoside is reported to be useful for preventing aging induced by D-galactose (D-gal). However, therapeutic mechanisms remain unclear. We thereby aimed to verify whether hyperoside, compared to vitamin E (VE), could alleviate renal aging and injury by regulating autophagic activity and its related signaling pathways. In vivo, rats were administered with either hyperoside or VE after renal aging modeling induced by D-gal. Changes in renal aging and injury markers, autophagic activity and AMPK-ULK1 signaling pathway in the kidneys were analysed. In vitro, the NRK-52E cells exposed to D-gal were used to investigate regulative actions of hyperoside and VE on cell viability, renal tubular cellular aging markers, autophagic activity and its related signaling pathways by histomorphometry, immunohistochemistry, immunofluorescence, lentiviral transfection and Western blot. Aging and injury in the kidneys and renal tubular cells induced by D-gal were ameliorated by hyperoside and VE. Hyperoside and VE inhibited autophagic activity through mTOR-independent and AMPK-ULK1 signaling pathways. Hyperoside, as a component of phytomedicine similar to VE, attenuated renal aging and injury induced by D-gal via inhibiting AMPK-ULK1-mediated autophagy. This study provides the first evidence that hyperoside contributes to the prevention of age-associated renal injury.