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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 7584691, 10 pages
Research Article

Resveratrol Prevents ROS-Induced Apoptosis in High Glucose-Treated Retinal Capillary Endothelial Cells via the Activation of AMPK/Sirt1/PGC-1α Pathway

1Department of Ophthalmology, Lishui Central Hospital, Fifth Affiliated Hospital of Wenzhou Medical University, Lishui, China
2Department of Ophthalmology, Lishui Hospital Affiliated with Zhejiang University, Lishui, China
3Department of Stomatology, Lishui Hospital Affiliated with Zhejiang University, Lishui, China

Correspondence should be addressed to Peipei Wang

Received 15 May 2017; Revised 17 July 2017; Accepted 6 August 2017; Published 29 October 2017

Academic Editor: Giuseppe Valacchi

Copyright © 2017 Jun Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Resveratrol (RSV) is used as a protective therapy against diabetic retinopathy. However, the mechanism(s) underlying this protective effect has not been fully elucidated. Bovine retinal capillary endothelial cells (BRECs), an in vitro model, were used to investigate the mechanism of RSV. Our results showed that high glucose induced significant cellular apoptosis in BRECs, which was accompanied by increased intracellular levels of reactive oxygen species (ROS) and cleaved caspase-3. The glucose-induced apoptosis and ROS elevation were both inhibited by RSV. High glucose was found to decrease the levels of phosphorylated AMP-activated protein kinase (p-AMPK), which was accompanied by increased levels of Sirt1 and PGC-1α. These changes were reversed by RSV. We also demonstrated that AMPK regulates the modulations of Sirt1 and PGC-1α using specific inhibitors of AMPK and Sirt1 and small interfering RNAs of PGC-1α. In summary, the current study demonstrates that RSV is effective against high glucose-induced cellular apoptosis and its action is exerted via the inhibition of ROS/AMPK/Sirt1/PGC-1α pathway.