ReferenceID 2603

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

Food Funct

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

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Reference Id
2603
Evidence Id
19193
Core Evidence Id
19193
Source Reference Id
5207
Herb2 Reference Id
HBREF006004
Subject Paper Key
HBIN039576_32195489
Pubmed Id
32195489
Doi
10.1039/c9fo02334h
Paper Title
Activation of AMPK/Sirt3 pathway by phloretin reduces mitochondrial ROS in vascular endothelium by increasing the activity of MnSOD via deacetylation
Paper 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 muM) 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.
Journal
Food Funct
Publish Year
2020
Experiment Subject
mouse
Experiment Type
Animal Experiment
Phenotype Related
Paper Title Cn
Paper Title En
Activation of AMPK/Sirt3 pathway by phloretin reduces mitochondrial ROS in vascular endothelium by increasing the activity of MnSOD via deacetylation
Bilingual Status
semi_complete