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Nutrients 2016, 8(12), 799; doi:10.3390/nu8120799

Regressive Effect of Myricetin on Hepatic Steatosis in Mice Fed a High-Fat Diet

1
Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China
2
State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, China
3
COFCO Corporation Oilseeds Processing Division, Beijing 100020, China
*
Author to whom correspondence should be addressed.
Received: 9 October 2016 / Revised: 4 December 2016 / Accepted: 5 December 2016 / Published: 11 December 2016
(This article belongs to the Special Issue Antioxidants in Health and Disease)
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Abstract

Myricetin is an effective antioxidant in the treatment of obesity and obesity-related metabolic disorders. The objective of this study was to explore the regressive effect of myricetin on pre-existing hepatic steatosis induced by high-fat diet (HFD). C57BL/6 mice were fed either a standard diet or a HFD for 12 weeks and then half of the mice were treated with myricetin (0.12% in the diet, w/w) while on their respective diets for further 12 weeks. Myricetin treatment significantly alleviated HFD-induced steatosis, decreased hepatic lipid accumulation and thiobarbituric acid reactive substance (TBARS) levels, and increased antioxidative enzyme activities, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Microarray analysis of hepatic gene expression profiles showed that myricetin significantly altered the expression profiles of 177 genes which were involved in 12 biological pathways, including the peroxisome proliferator activated receptor (PPAR) signaling pathway and peroxisome. Further research indicated that myricetin elevated hepatic nuclear Nrf2 translocation, increased the protein expression of heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1), reduced the protein expression of PPARγ, and normalized the expressions of genes that were involved in peroxisome and the PPAR signaling pathway. Our data indicated that myricetin might represent an effective therapeutic agent to treat HFD-induced hepatic steatosis via activating the Nrf2 pathway and the PPAR signaling pathway. View Full-Text
Keywords: myricetin; hepatic steatosis; Nrf2; PPARγ; oxidative stress myricetin; hepatic steatosis; Nrf2; PPARγ; oxidative stress
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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. (CC BY 4.0).

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MDPI and ACS Style

Xia, S.-F.; Le, G.-W.; Wang, P.; Qiu, Y.-Y.; Jiang, Y.-Y.; Tang, X. Regressive Effect of Myricetin on Hepatic Steatosis in Mice Fed a High-Fat Diet. Nutrients 2016, 8, 799.

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