Lychee pulp phenolics ameliorate hepatic lipid accumulation by reducing miR-33 and miR-122 expression in mice fed a high-fat diet
Lychee pulp phenolics ameliorate hepatic lipid accumulation by reducing miR-33 and miR-122 expression in mice fed a high-fat diet
复制标题
荔枝果肉酚类物质通过降低高脂饮食小鼠的 miR-33 和 miR-122 表达来改善肝脏脂质积累
DOI：
10.1039/c6fo01507g
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发表时间：
2017-02-01
期刊：
影响因子：
6.1
通讯作者：
Zhang, Mingwei
中科院分区：
文献类型：
--
作者：
Su, Dongxiao;Zhang, Ruifen;Zhang, Mingwei
饮食酚类通过改变脂质代谢相关的microRNA（miRNA）表达表现出低脂肪性活性。槲皮素3-O-Rutinoside-7-O-Alpha-Lhamnosidase（槲皮素3-RUT-7-RHA），鲁丁蛋白和（ - ） - epicatechin是Lychee（Litchi Chinensis sonn。）的主要酚类。先前的一项研究报告说，槲皮素3-RUT-7-RHA和鲁丁蛋白具有降脂性作用。为了阐明这些作用以及乳脂酚（LPP）的潜在分子机制，仅在用高脂饮食（HFD）治疗十周后测量了脂质代谢相关基因的肝mRNA和蛋白质表达及其相关的miRNA或与LPP结合使用。 LPP的给药显着降低了HFD诱导的血清总胆固醇和甘油三酸酯水平的增加，但增加了HDL-C含量。肝腺苷三磷酸盒结合盒转运蛋白A1（ABCA1）和肉碱棕榈酰转移酶1A（CPT1A）的mRNA和蛋白质表达水平上调，而脂肪酸合成酶（FAS）mRNA（FAS）mRNA和相应的蛋白质表达水平被LPPs下调。此外，直接调节ABCA1和CPT1A和MiR-122的miR-33的表达水平间接调节Fas，在小鼠肝细胞中下调。 miR-33和miR-122的抑制是LPP在肝脏中降低脂质性作用的可能分子机制。我们的结果表明LPP的一种新型降低脂质性机制。
Dietary phenolics exhibit hypolipidemic activity by changing lipid metabolism-related microRNA (miRNA) expression. Quercetin 3-O-rutinoside-7-O-alpha-L-rhamnosidase (quercetin 3-rut-7-rha), rutin and (-)-epicatechin are the main phenolics in lychee (Litchi chinensis Sonn.) pulp. A previous study reported that quercetin 3-rut-7-rha and rutin had hypolipidemic effects. To elucidate these effects and the underlying molecular mechanisms of lychee pulp phenolics (LPPs), the hepatic mRNA and protein expression of lipid metabolism-related genes and their associated miRNAs were measured after ten weeks of treatment with a high-fat diet (HFD) alone or in combination with LPPs. The administration of LPPs significantly reduced the HFD-induced increase in serum total cholesterol and triglyceride levels but increased the HDL-c content. The mRNA and protein expression levels of hepatic adenosine triphosphate-binding cassette transporter A1 (ABCA1) and carnitine palmitoyltransferase 1a (CPT1a) were upregulated, while fatty acid synthase (FAS) mRNA and the corresponding protein expression levels were downregulated by LPPs. Furthermore, the expression levels of miR-33, which directly modulates ABCA1 and CPT1a, and miR-122, which indirectly regulates FAS, were downregulated in mouse hepatocytes. The repression of miR-33 and miR-122 is a possible molecular mechanism of the hypolipidemic effects of LPPs in the liver. Our results suggest a novel hypolipidemic mechanism of LPPs.