基础医学论著

短链脂肪酸对HepG2细胞脂质堆积模型脂质代谢的影响*

  • 郭宇帆 ,
  • 高冰 ,
  • 姜红梅 ,
  • 商佳琪 ,
  • 高龙 ,
  • 赵宇航 ,
  • 田春风 ,
  • 李凯 ,
  • 包艳
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  • 1.包头医学院公共卫生学院,内蒙古包头 014040;
    2.包头医学院营养与食品健康研究所

收稿日期: 2022-09-13

  网络出版日期: 2023-03-08

基金资助

*高校青年科技英才项目(NJYT22119);国家自然科学基金(81560150);内蒙古自治区自然科学基金(2021LHMS08017),自治区卫生健康科技计划项目(202201368)

Effects of short-chain fatty acids on lipid metabolism in HepG2 cell lipid accumulation model

  • GUO Yufan ,
  • GAO Bing ,
  • JIANG Hongmei ,
  • SHANG Jiaqi ,
  • GAO Long ,
  • ZHAO Yuhang ,
  • TIAN Chunfeng ,
  • LI Kai ,
  • BAO Yan
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  • 1. School of Public Health, Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou 014040, China;
    2. Institute of Nutrition and Food Health, Baotou Medical College, Inner Mongolia University of Science and Technology

Received date: 2022-09-13

  Online published: 2023-03-08

摘要

目的: 揭示肠道菌群产物短链脂肪酸(Short-chain fatty acids,SCFAs)对HepG2细胞脂质堆积模型脂质代谢的影响。方法: 通过油红O染色法观察油酸钠建立的HepG2细胞脂质堆积模型,使用不同浓度的SCFAs(乙酸、丙酸、正丁酸)干预HepG2细胞脂质堆积模型,MTT法检测HepG2细胞存活率;TC、TG试剂盒检测HepG2细胞脂质堆积模型中TC、TG含量;Western blot检测HepG2细胞AMPK、p-AMPK、ACC和p-ACC等蛋白的表达量。结果: 随着三种SCFAs浓度的升高,HepG2细胞活性逐渐降低(P<0.05);SCFAs干预HepG2细胞脂质堆积模型后TC、TG含量降低(P<0.05),并抑制脂质堆积模型组细胞内AMPK、ACC的磷酸化表达。结论: SCFAs对HepG2细胞活性、HepG2细胞脂质堆积模型脂质代谢以及蛋白表达均有影响,不同浓度不同种类的SCFAs干预结果有差异。

本文引用格式

郭宇帆 , 高冰 , 姜红梅 , 商佳琪 , 高龙 , 赵宇航 , 田春风 , 李凯 , 包艳 . 短链脂肪酸对HepG2细胞脂质堆积模型脂质代谢的影响*[J]. 包头医学院学报, 2023 , 39(2) : 1 -6 . DOI: 10.16833/j.cnki.jbmc.2023.02.001

Abstract

Objective: To evaluate the effect of short-chain fatty acids (SCFAs) produced by intestinal flora on lipid metabolism in HepG2 cell lipid accumulation model. Methods: The lipid accumulation model of HepG2 cells was observed by oil red O staining. Different concentrations of SCFAs (acetic acid, propionic acid and n-butyric acid) were used to intervene the lipid accumulation model of HepG2 cells. The survival rate of HepG2 cells was detected by MTT method. TC and TG contents in HepG2 cell lipid accumulation model were detected by TC and TG kits. Western blot was used to detect the expression of AMPK, p-AMPK, ACC and p-ACC in HepG2 cells. Results: The activity of HepG2 cells gradually decreased with the increase of three concentrations of SCFAs ( P<0.05). After intervention with SCFAs in the lipid accumulation model of HepG2 cells, the contents of TC and TG were decreased (P<0.05), and the phosphorylation of AMPK and ACC in the lipid accumulation model group was inhibited. Conclusion: SCFAs affects the HepG2 cell activity, lipid metabolism and protein expression in HepG2 cell lipid accumulation model, and the intervention results of SCFAs under different concentrations and types are different.

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