• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

利用张氏肝细胞建立肝细胞脂肪变性模型。

Establishment of a hepatocyte steatosis model using Chang liver cells.

作者信息

Yan D, Dou Q L, Wang Z, Wei Y Y

机构信息

Department of Pharmacology, Basic Medical College, Xinjiang Medical University, Xinjiang, China.

ICU, The First Affiliated Hospital of Xinjiang Medical University, Xinjiang, China.

出版信息

Genet Mol Res. 2015 Nov 26;14(4):15224-32. doi: 10.4238/2015.November.25.10.

DOI:10.4238/2015.November.25.10
PMID:26634485
Abstract

The objective of this study was to explore the experimental conditions for hepatocellular steatosis models of Chang liver cells induced by oleic acid (OA). For that, Chang liver cells were induced by different concentrations of OA for different periods. The MTT assay was used to detect hepatic cell activity, the Oil Red O staining was used to observe intracellular lipid droplets accumulation, and the glycerol phosphate oxidase method was used to detect the triglyceride (TG) content in the Chang liver cell. The hepatocellular steatosis models of Chang liver cell were established successfully by inducing with 0.2 mM OA for 24h. TG content in model cells was 379.98 ± 23.19 mg/g, which is significantly different from control cells (185.03 ± 12.68 mg/g; P < 0.01). These were considered proper conditions for establishing hepatocellular steatosis models of Chang liver cells, producing a reliable model for nonalcoholic fatty liver disease research.

摘要

本研究的目的是探索油酸(OA)诱导Chang肝细胞发生肝细胞脂肪变性模型的实验条件。为此,用不同浓度的OA对Chang肝细胞诱导不同时间。采用MTT法检测肝细胞活性,用油红O染色观察细胞内脂滴积累情况,并用磷酸甘油氧化酶法检测Chang肝细胞内甘油三酯(TG)含量。用0.2 mM OA诱导24小时成功建立了Chang肝细胞的肝细胞脂肪变性模型。模型细胞中TG含量为379.98±23.19 mg/g,与对照细胞(185.03±12.68 mg/g;P<0.01)有显著差异。这些被认为是建立Chang肝细胞脂肪变性模型的合适条件,为非酒精性脂肪性肝病研究提供了可靠的模型。

相似文献

1
Establishment of a hepatocyte steatosis model using Chang liver cells.利用张氏肝细胞建立肝细胞脂肪变性模型。
Genet Mol Res. 2015 Nov 26;14(4):15224-32. doi: 10.4238/2015.November.25.10.
2
[Expression and significance of insulin-like growth factor-1 and insulin-like growth factor binding protein-3 in hepatocyte steatosis model].[胰岛素样生长因子-1及胰岛素样生长因子结合蛋白-3在肝细胞脂肪变性模型中的表达及意义]
Zhonghua Gan Zang Bing Za Zhi. 2012 Mar;20(3):196-200. doi: 10.3760/cma.j.issn.1007-3418.2012.03.012.
3
[Effects of PPAR-alpha activation on oleic acid-induced steatosis and expression of heme oxygenase-1 in HepG2 cells].[过氧化物酶体增殖物激活受体α激活对油酸诱导的HepG2细胞脂肪变性及血红素加氧酶-1表达的影响]
Zhonghua Gan Zang Bing Za Zhi. 2013 Mar;21(3):218-21.
4
Oleic acid-induced hepatic steatosis is coupled with downregulation of aquaporin 3 and upregulation of aquaporin 9 via activation of p38 signaling.油酸诱导的肝脂肪变性与水通道蛋白3的下调以及通过p38信号通路激活导致的水通道蛋白9的上调相关联。
Horm Metab Res. 2015 Apr;47(4):259-64. doi: 10.1055/s-0034-1384569. Epub 2014 Aug 8.
5
A human hepatocellular in vitro model to investigate steatosis.一种用于研究脂肪变性的人肝细胞体外模型。
Chem Biol Interact. 2007 Jan 30;165(2):106-16. doi: 10.1016/j.cbi.2006.11.004. Epub 2006 Nov 23.
6
Prolyl Oligopeptidase Inhibition Attenuates Steatosis in the L02 Human Liver Cell Line.脯氨酰寡肽酶抑制可减轻L02人肝细胞系中的脂肪变性。
PLoS One. 2016 Oct 19;11(10):e0165224. doi: 10.1371/journal.pone.0165224. eCollection 2016.
7
Biomechanics of cultured hepatic cells during different steatogenic hits.培养肝细胞在不同成脂刺激下的生物力学特性。
J Mech Behav Biomed Mater. 2019 Sep;97:296-305. doi: 10.1016/j.jmbbm.2019.05.036. Epub 2019 May 22.
8
Differential effect of oleic and palmitic acid on lipid accumulation and apoptosis in cultured hepatocytes.油酸和棕榈酸对培养肝细胞脂质积累和凋亡的差异作用。
J Gastroenterol Hepatol. 2009 May;24(5):830-40. doi: 10.1111/j.1440-1746.2008.05733.x. Epub 2009 Jan 13.
9
[Establishment and optimization of hepatocyte steatosis model].[肝细胞脂肪变性模型的建立与优化]
Zhonghua Gan Zang Bing Za Zhi. 2018 Dec 20;26(12):922-926. doi: 10.3760/cma.j.issn.1007-3418.2018.12.009.
10
Inhibition of exendin-4-induced steatosis by protein kinase A in cultured HepG2 human hepatoma cells.蛋白激酶A对培养的HepG2人肝癌细胞中艾塞那肽-4诱导的脂肪变性的抑制作用。
In Vitro Cell Dev Biol Anim. 2017 Sep;53(8):721-727. doi: 10.1007/s11626-017-0181-y. Epub 2017 Jul 13.

引用本文的文献

1
Sodium butyrate attenuates lipid metabolism disorder via improving mitochondrial function and activating autophagy in LMH cells.丁酸钠通过改善线粒体功能和激活LMH细胞自噬来减轻脂质代谢紊乱。
Poult Sci. 2025 Jun 25;104(9):105476. doi: 10.1016/j.psj.2025.105476.
2
3,5-Dimethyl-2,4,6-trimethoxychalcone Lessens Obesity and MAFLD in Leptin-Deficient Mice.3,5-二甲基-2,4,6-三甲氧基查尔酮可减轻瘦素缺乏小鼠的肥胖和 MAFLD。
Int J Mol Sci. 2024 Sep 11;25(18):9838. doi: 10.3390/ijms25189838.
3
Oleic acid-induced steatosis model establishment in LMH cells and its effect on lipid metabolism.
油酸钠诱导 LMH 细胞脂肪变性模型的建立及其对脂代谢的影响。
Poult Sci. 2023 Jan;102(1):102297. doi: 10.1016/j.psj.2022.102297. Epub 2022 Oct 29.
4
Protein Profiling of a Cellular Model of NAFLD by Advanced Bioanalytical Approaches.采用先进的生物分析方法对非酒精性脂肪性肝病的细胞模型进行蛋白质组学分析。
Int J Mol Sci. 2022 Aug 12;23(16):9025. doi: 10.3390/ijms23169025.
5
Menin regulates lipid deposition in mouse hepatocytes via interacting with transcription factor FoxO1.Menin 通过与转录因子 FoxO1 相互作用调节小鼠肝细胞中的脂质沉积。
Mol Cell Biochem. 2022 May;477(5):1555-1568. doi: 10.1007/s11010-022-04392-6. Epub 2022 Feb 19.
6
Hepatocyte steatosis inhibits hepatitis B virus secretion via induction of endoplasmic reticulum stress.肝细胞脂肪变性通过诱导内质网应激抑制乙型肝炎病毒的分泌。
Mol Cell Biochem. 2022 Nov;477(11):2481-2491. doi: 10.1007/s11010-021-04143-z. Epub 2021 May 13.
7
Switching from Fatty Acid Oxidation to Glycolysis Improves the Outcome of Acute-On-Chronic Liver Failure.从脂肪酸氧化转变为糖酵解可改善慢加急性肝衰竭的预后。
Adv Sci (Weinh). 2020 Feb 13;7(7):1902996. doi: 10.1002/advs.201902996. eCollection 2020 Apr.
8
Best practices for naming, receiving, and managing cells in culture.培养物中细胞命名、接收和管理的最佳实践。
In Vitro Cell Dev Biol Anim. 2017 Oct;53(9):761-774. doi: 10.1007/s11626-017-0199-1. Epub 2017 Oct 6.