Influence of total polar compounds on lipid metabolism, oxidative stress and cytotoxicity in HepG2 cells

被引:21
作者
Ju, Jingjie [1 ]
Zheng, Zhaojun [1 ]
Xu, Yong-jiang [1 ]
Cao, Peirang [1 ]
Li, Jingwei [1 ]
Li, Qiu [2 ]
Liu, Yuanfa [1 ]
机构
[1] Jiangnan Univ, Sch Food Sci & Technol, Collaborat Innovat Ctr Food Safety & Qual Control, Natl Engn Lab Cereal Fermentat Technol, 1800 Lihu Rd, Wuxi 214122, Jiangsu, Peoples R China
[2] Shandong LuHua Grp Co LTD, Laiyang 265200, Peoples R China
基金
国家重点研发计划; 美国国家科学基金会;
关键词
Total polar compounds (TPC); Lipid metabolism; Oxidation stress; HepG2; cell; TRIGLYCERIDE TRANSFER PROTEIN; FATTY LIVER; NUCLEAR RECEPTORS; BIOMARKER; MODEL;
D O I
10.1186/s12944-019-0980-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
BackgroundRecently, the harmful effects of frying oil on health have been gradually realized. However, as main components of frying oils, biochemical effects of total polar compounds (TPC) on a cellular level were underestimated.MethodsThe effects of total polar compounds (TPC) in the frying oil on the lipid metabolism, oxidative stress and cytotoxicity of HepG2 cells were investigated through a series of biochemical methods, such as oil red staining, real-time polymerase chain reaction (RT-PCR), cell apoptosis and cell arrest.ResultsHerein, we found that the survival rate of HepG2 cells treated with TPC decreased in a time and dose dependent manner, and thereby presented significant lipid deposition over the concentration of 0.5mg/mL. TPC were also found to suppress the expression levels of PPAR, CPT1 and ACOX, elevate the expression level of MTP and cause the disorder of lipid metabolism. TPC ranged from 0 to 2mg/mL could significantly elevate the amounts of reactive oxygen species (ROS) in HepG2 cells, and simultaneously increase the malondialdehyde (MDA) content from 21.212.62 to 65.71 +/- 4.20mol/mg of protein (p<0.05) at 24h. On the contrary, antioxidant enzymes superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) respectively decreased by 0.52-, 0.56- and 0.28-fold, when HepG2 cells were exposed to 2mg/mL TPC for 24h. In addition, TPC could at least partially induce the apoptosis of HepG2 cells, and the transition from G0/G1 to G2 phase in HepG2 cells was impeded.Conclusions< TPC could progressively cause lipid deposition, oxidative stress and cytotoxicity, providing the theoretical support for the detrimental health effects of TPC.
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页数:13
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