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来自[具体事物]的汁液可使饮食诱导的高脂血症小鼠的血脂正常化*。 (注:原文中“Juice from”后面缺少具体内容)

Juice from normalizes blood lipids in mice with diet-induced hyperlipidemia*.

作者信息

Song Pingping, Shen Xiangchun

机构信息

The State Key Laboratory of Functions and Applications of Medicinal Plants Guizhou Medical University Guiyang China.

Key Laboratory of Optimal Utilization of Natural Medicine Resources School of Pharmaceutical Sciences Guizhou Medical University Guiyang China.

出版信息

Food Sci Nutr. 2020 Sep 18;8(11):6069-6082. doi: 10.1002/fsn3.1897. eCollection 2020 Nov.

Abstract

(FRR) as a dietary supplement is considered to possess anti-atherosclerosis (AS), and hyperlipidemia (HLP) is material basis for AS formation, so the effects and molecular mechanism of FRR on diet-induced hyperlipidemic mice were explored. In Diet IV2 group, hepatic steatosis was significantly relieved; meanwhile, TC, TG, LDL-C, HDL-C, and ASI in serum were regulated to control level. Thirty-seven DCEG in Diet I, Diet II, and Diet IV2 groups were obtained by RNA-seq analysis. Relative mRNA levels were further determined by qRT-PCR, of which 28 genes were matched with those detected by RNA-seq. Ten DCEP were verified by targeted quantitative proteomic analysis, but expressive patterns of only six proteins were correlated with qRT-PCR data. These DCEG and DCEP played important roles in regulating the biosynthesis of BAs and steroids, fatty acid metabolism, and LPO production. They might cooperatively regulate the function of HDL or RCT by PPAR signaling pathway under the FRR action. As we know, it is the first time the potential anti-atherosclerotic mechanism of FRR regulating the blood lipids was explored.

摘要

(FRR)作为一种膳食补充剂被认为具有抗动脉粥样硬化(AS)作用,而高脂血症(HLP)是AS形成的物质基础,因此探讨了FRR对饮食诱导的高脂血症小鼠的影响及其分子机制。在饮食IV2组中,肝脂肪变性明显减轻;同时,血清中的总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)和动脉粥样硬化指数(ASI)被调节至对照水平。通过RNA测序分析在饮食I、饮食II和饮食IV2组中获得了37个差异表达基因(DCEG)。通过qRT-PCR进一步测定相对mRNA水平,其中28个基因与RNA测序检测到的基因匹配。通过靶向定量蛋白质组学分析验证了10个差异表达蛋白(DCEP),但只有6种蛋白质的表达模式与qRT-PCR数据相关。这些DCEG和DCEP在调节胆汁酸和类固醇的生物合成、脂肪酸代谢以及脂质过氧化产物(LPO)生成中发挥重要作用。它们可能在FRR作用下通过过氧化物酶体增殖物激活受体(PPAR)信号通路协同调节高密度脂蛋白(HDL)的功能或逆向胆固醇转运(RCT)。据我们所知,这是首次探索FRR调节血脂的潜在抗动脉粥样硬化机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2fa/7684604/414ae0aa1d73/FSN3-8-6069-g001.jpg

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