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Activation of AMPK/Sirt3 pathway by phloretin reduces mitochondrial ROS in vascular endothelium by increasing the activity of MnSOD via deacetylation

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Abstract

As a dihydrochalcone, phloretin was reported to effectively attenuate palmitic acid (PA)-induced oxidative stress in endothelial cells. In the present study, we further investigated the antioxidant capacity of phloretin via restoring the activity of MnSOD through deacetylation in vitro and in vivo. The results revealed that phloretin (50 μM) treatment significantly increased the activity of MnSOD in the HUVECs and mouse aortas, and then obviously reduced the accumulation of mitochondrial ROS. Immunoprecipitation assay and Western blot analysis indicated that phloretin could decrease the lysine acetylation of MnSOD and restore its activity by promoting the expression of Sirt3 by increasing the phosphorylation of AMPK (Thr172). These findings provide a novel profile to explain the antioxidant activity of phloretin by reducing the acetylation level of MnSOD via an AMPK/Sirt3 signaling pathway.

Graphical abstract: Activation of AMPK/Sirt3 pathway by phloretin reduces mitochondrial ROS in vascular endothelium by increasing the activity of MnSOD via deacetylation

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Article information


Submitted
06 Oct 2019
Accepted
15 Feb 2020
First published
19 Feb 2020

Food Funct., 2020, Advance Article
Article type
Paper

Activation of AMPK/Sirt3 pathway by phloretin reduces mitochondrial ROS in vascular endothelium by increasing the activity of MnSOD via deacetylation

L. Han, J. Li, J. Li, C. Pan, Y. Xiao, X. Lan and M. Wang, Food Funct., 2020, Advance Article , DOI: 10.1039/C9FO02334H

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