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Article Publish Status: FREE
Abstract Title:

(-)-Epigallocatechin-3-Gallate Ameliorates Atherosclerosis and Modulates Hepatic Lipid Metabolic Gene Expression in Apolipoprotein E Knockout Mice: Involvement of TTC39B.

Abstract Source:

Front Pharmacol. 2018 ;9:195. Epub 2018 Mar 9. PMID: 29593532

Abstract Author(s):

Li-Long Pan, Yan Wu, Ru-Qing Wang, Jin-Wu Chen, Jing Chen, Yan Zhang, Ya-Jun Chen, Ming Geng, Zhong-Dong Xu, Min Dai, Jin-Hua Li, Wei Wang, Zheng-Zhu Zhang

Article Affiliation:

Li-Long Pan

Abstract:

Aberrant chronic inflammation and excess accumulation of lipids play a pivotal role in the occurrence and progression of atherosclerosis. (-)-Epigallocatechin-3-gallate (EGCG), the major catechins in green tea, displayed anti-atherosclerotic propertiesand. However, the effects and underlying mechanism of EGCG on atherosclerosis remain unclear.Male apolipoprotein E-knockout (ApoE) mice (7 weeks old) fed with high-fat diet (HFD) were treated with normal saline or EGCG (40 mg/kg/d, i.g.) for 18 weeks. Atherosclerotic plaque and liver lipid accumulation were measured by Oil Red staining. Plasma lipids and cytokines were detected using commercial kits. The expression of protein and mRNA was analyzed by western blot and quantitative real-time reverse transcription-polymerase chain reaction, respectively.EGCG administration markedly attenuated atherosclerotic plaque formation in HFD-fed ApoEmice, which were accompanied by increased plasma interleukin-10 (IL-10) level and decreased plasma IL-6 and tumor necrosis factor-α (TNF-α) levels. In addition, EGCG modulated high-fat-induced dyslipidemia, evidencing by decreased total cholesterol (TC) and low-density lipoprotein levels and increased high-density lipoprotein level. Meanwhile, EGCG treatment alleviated high-fat-mediated liver lipid accumulation and decreasedliver TC and triglyceride. Mechanistically, EGCG significantly modulated high-fat-induced hepatic tetratricopeptide repeat domain protein 39B (TTC39B) expression and its related genes () expression in liver from ApoEmice. Notably, EGCG remarkably induced hepatic liver X receptorα (LXRα) and LXRβ expression and inhibited both precursor and mature sterol regulatory element binding transcription factor-1 (SREBP-1) expression.Taken together, our data for the first time suggested that TTC39B was involved in EGCG-mediated anti-atherosclerotic effects through modulation of LXR/SREBP-1 pathway.

Study Type : Animal Study

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Sayer Ji
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