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Regressive Effect of Myricetin on Hepatic Steatosis in Mice Fed a High-Fat Diet
- Xia, Shu-Fang, Le, Guo-Wei, Wang, Peng, Qiu, Yu-Yu, Jiang, Yu-Yu, Tang, Xue
- Nutrients 2016 v.8 no.12
- NAD(P)H dehydrogenase (quinone), antioxidant enzymes, catalase, enzyme activity, fatty liver, gene expression, genes, glutathione peroxidase, heme oxygenase (biliverdin-producing), high fat diet, lipids, metabolic diseases, mice, microarray technology, myricetin, obesity, peroxisome proliferator-activated receptor gamma, protein synthesis, quinones, signal transduction, superoxide dismutase, therapeutics, thiobarbituric acid-reactive substances
- 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.