文献类型：期刊文献

中文题名：牛磺酸对HepG2细胞甘油三酯合成的影响研究

英文题名：Effect of taurine on triglyceride synthesis in HepG2 cells

作者：马于巽[1];宋琪[1];张静[1,2];郭俊霞[1,2];夏天则[2];陈文[1,2]

第一作者：马于巽

机构：[1]北京联合大学生物活性物质与功能食品北京市重点实验室,北京100191;[2]北京联合大学生物化学工程学院食品科学系,北京100023

第一机构：北京联合大学应用文理学院

年份：2020

卷号：32

期号：5

起止页码：867-873

中文期刊名：天然产物研究与开发

外文期刊名：Natural Product Research and Development

收录：CSTPCD;;北大核心:【北大核心2017】；CSCD:【CSCD2019_2020】；

基金：北京联合大学生物活性物质与功能食品北京市重点实验室开放课题(122139918290104056)。

语种：中文

中文关键词：牛磺酸;甘油三酯;固醇调节元件结合蛋白1c

外文关键词：taurine;triglyceride;SREBP-1c

摘要：本文探讨牛磺酸对HepG2细胞甘油三酯合成的影响,为牛磺酸预防/改善机体高脂状态的深入研究提供参考。在DMEM培养基中添加0.05 mmol/L油酸建立高甘油三酯细胞模型,分别以终浓度为1、5、10、20 mmol/L的牛磺酸处理细胞24、48、72 h,测定细胞内甘油三酯水平;并检测5 mmol/L牛磺酸作用24 h后细胞内固醇调节元件结合蛋白1c(SREBP-1c)及脂肪合成相关酶乙酰辅酶A合成酶(AceCS)、乙酰辅酶A羧化酶(ACC)、脂肪酸合成酶(FAS)、长链酰基辅酶A合成酶1(ACSL1)的蛋白表达水平。1 mmol/L牛磺酸作用72 h,5和10 mmol/L牛磺酸作用24、48、72 h,20 mmol/L牛磺酸作用24和48 h均可使高脂HepG2细胞内甘油三酯水平显著下降(P<0.05);5 mmol/L牛磺酸作用24 h,高脂HepG2细胞的SREBP-1c、FAS、ACC、AceCS1、ACSL1表达明显减少(P<0.05),磷酸化ACC表达显著增加(P<0.05)。结论:牛磺酸通过调控SREBP-1c及其下游靶基因而抑制高脂HepG2细胞脂肪酸/甘油三酯的合成。
The effect of taurine on triglyceride synthesis and its preliminary mechanism in oleic acid-treated HepG2 cells was researched in this article.A high triglyceride cell model was established by adding 0.05 mmol/L oleic acid to DMEM medium.HepG2 cells were treated with taurine at final concentration of 1,5,10 and 20 mmol/L for 24,48 and 72 h,and the levels of intracellular triglycerides were determined.The expression of SREBP-1c and the enzymes of AceCS1,ACC,FAS and ACSL1,associated with fatty acid synthesis,were detected by western blot after HepG2 cells were incubated with 5 mmol/L taurine for 24 h.Intracellular triglycerides levels were decreased by 1 mmol/L taurine treatment for 72 h(P<0.05),5 and 10 mmol/L taurine treatment for 24/48/72 h(P<0.05)and 20 mmol/L taurine treatment for 24/48 h(P<0.05)in high-triglyceride cells.And the protein expression of SREBP-1c,FAS,ACC,AceCS1 and ACSL1 were reduced while p-ACC was increased by 5 mmol/L taurine treatment for 24 h(P<0.05).Taurine inhibits the synthesis of fatty acid/triglyceride in oleic acid-treated HepG2 cells by regulating SREBP-1c and its downstream genes.