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Int. J. Mol. Sci. 2016, 17(11), 1932;

Isoliquiritigenin Attenuates Atherogenesis in Apolipoprotein E-Deficient Mice

Department of Biochemistry and Molecular Biology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University School of Basic Medical Sciences, 185 Donghu Road, Bldg. 2, 2-209, Wuhan 430071, China
Medical College, Tibet University, Lhasa 850000, China
Department of Pharmacy, Zhongnan Hospital of Wuhan University, Wuhan 430071, China
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Shaker A. Mousa
Received: 28 August 2016 / Revised: 9 November 2016 / Accepted: 11 November 2016 / Published: 18 November 2016
(This article belongs to the Special Issue Vascular Biology and Therapeutics)
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Isoliquiritigenin (ISL) exhibits antioxidation and anti-inflammation activity. We sought to investigate the effects and mechanism of ISL on the development of atherosclerotic lesions in apolipoprotein E-deficient (apoE−/−) mice. Firstly, we determined that ISL reduced the mRNA levels of inflammatory factors interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and monocyte chemotactic protein-1 (MCP-1), while it increased the expression of several lipoprotein-related genes in peritoneal macrophages treated with lipopolysaccharide (LPS). ISL also enhanced peroxisome proliferator-activated receptor gamma (PPARγ) protein levels and reversed the changes of ATP-binding cassette transporter A (ABCA1) and cluster of differentiation 36 (CD36) in macrophages treated with oxidative low-density lipoprotein (ox-LDL). Then, in an in vivo study, female apoE−/− mice were fed a Western diet with ISL (0, 20, 100 mg/kg/day) added for 12 weeks. We found that ISL decreased the plasma cholesterol levels of very low-density lipoprotein (VLDL)/LDL, promoted plasma superoxide dismutase (SOD) and paraoxonase-1 (PON1) activities, and decreased plasma IL-6, TNF-α, and MCP-1 levels. Moreover, ISL significantly reduced the atherosclerotic lesions and hepatic steatosis in apoE−/− mice. In the liver, ISL altered the expression of several key genes (such as SRBI, ABCA1, ABCG8, PPARγ, and FASN) involving cholesterol-selective uptake and excretion into bile, triglyceride (TG) biosynthesis, and inflammation. These results suggest that the atheroprotective effects of ISL are due to the improvement of lipid metabolism, antioxidation, and anti-inflammation, which involve PPARγ-dependent signaling. View Full-Text
Keywords: isoliquiritigenin; atherosclerosis; cholesterol flux; anti-inflammation; anti-oxidation isoliquiritigenin; atherosclerosis; cholesterol flux; anti-inflammation; anti-oxidation

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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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Du, F.; Gesang, Q.; Cao, J.; Qian, M.; Ma, L.; Wu, D.; Yu, H. Isoliquiritigenin Attenuates Atherogenesis in Apolipoprotein E-Deficient Mice. Int. J. Mol. Sci. 2016, 17, 1932.

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