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杨梅素增加大鼠肝过氧化物酶体增殖物激活受体α蛋白表达并降低血浆脂质和肥胖。

Myricetin Increases Hepatic Peroxisome Proliferator-Activated Receptor α Protein Expression and Decreases Plasma Lipids and Adiposity in Rats.

机构信息

School of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan.

出版信息

Evid Based Complement Alternat Med. 2012;2012:787152. doi: 10.1155/2012/787152. Epub 2012 Mar 8.

Abstract

The aim of this study was to investigate the antiobesity and antihyperlipidaemic effects of myricetin. Myricetin exhibited a significant concentration-dependent decrease in the intracellular accumulation of triglyceride in 3T3-L1 adipocytes. The high-fat diet (HFD)-fed rats were dosed orally with myricetin or fenofibrate, once daily for eight weeks. Myricetin (300 mg kg(-1) per day) displayed similar characteristics to fenofibrate (100 mg kg(-1) per day) in reducing lowered body weight (BW) gain, visceral fat-pad weights and plasma lipid levels of HFD-fed rats. Myricetin also reduced the hepatic triglyceride and cholesterol contents, as well as lowered hepatic lipid droplets accumulation and epididymal adipocyte size in HFD-fed rats. Myricetin and fenofibrate reversed the HFD-induced down-regulation of the hepatic peroxisome proliferator activated receptor (PPAR)α. HFD-induced decreases of the hepatic protein level of acyl-CoA oxidase and cytochrome P450 isoform 4A1 were up-regulated by myricetin and fenofibrate. The elevated expressions of hepatic sterol regulatory element binding proteins (SREBPs) of HFD-fed rats were lowered by myricetin and fenofibrate. These results suggest that myricetin suppressed BW gain and body fat accumulation by increasing the fatty acid oxidation, which was likely mediated via up-regulation of PPARα and down-regulation of SREBP expressions in the liver of HFD-fed rats.

摘要

本研究旨在探讨杨梅素的抗肥胖和抗高血脂作用。杨梅素在 3T3-L1 脂肪细胞中表现出显著的浓度依赖性甘油三酯细胞内积累减少。高脂饮食(HFD)喂养的大鼠每天口服给予杨梅素或非诺贝特,连续 8 周。杨梅素(每天 300mg/kg)在降低 HFD 喂养大鼠的体重(BW)增加、内脏脂肪垫重量和血浆脂质水平方面,与非诺贝特(每天 100mg/kg)具有相似的特征。杨梅素还降低了 HFD 喂养大鼠的肝甘油三酯和胆固醇含量,以及降低了肝内脂滴积累和附睾脂肪细胞大小。杨梅素和非诺贝特逆转了 HFD 诱导的肝过氧化物酶体增殖物激活受体(PPAR)α 的下调。HFD 诱导的酰基辅酶 A 氧化酶和细胞色素 P450 同工酶 4A1 的肝蛋白水平降低被杨梅素和非诺贝特上调。HFD 喂养大鼠肝固醇调节元件结合蛋白(SREBPs)的升高表达被杨梅素和非诺贝特降低。这些结果表明,杨梅素通过增加脂肪酸氧化来抑制 BW 增加和体脂肪积累,这可能是通过上调 PPARα 和下调 SREBP 在 HFD 喂养大鼠肝脏中的表达来介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4263/3310287/50f20f0411c4/ECAM2012-787152.001.jpg

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