The effects of di 2-ethyl hexyl phthalate (DEHP) on cellular lipid accumulation in HepG2 cells and its potential mechanisms in the molecular level

Autor: Wang Zhang, Wei Wei, Hao Chen, Weiping Xu, Xin yue Shen, Wen-wen Zhang
Rok vydání: 2016
Předmět:
0301 basic medicine
endocrine system
medicine.medical_specialty
Health
Toxicology and Mutagenesis

Cell Culture Techniques
Peroxisome proliferator-activated receptor
010501 environmental sciences
Toxicology
medicine.disease_cause
01 natural sciences
Superoxide dismutase
03 medical and health sciences
chemistry.chemical_compound
Plasticizers
Internal medicine
Diethylhexyl Phthalate
Malondialdehyde
medicine
Oil Red O
Humans
PPAR alpha
0105 earth and related environmental sciences
chemistry.chemical_classification
Microscopy
Confocal

biology
Dose-Response Relationship
Drug

Superoxide Dismutase
Phthalate
Hep G2 Cells
Lipid Metabolism
Sterol regulatory element-binding protein
Oleic acid
Oxidative Stress
030104 developmental biology
Endocrinology
chemistry
Biochemistry
biology.protein
Sterol Regulatory Element Binding Protein 1
Oxidative stress
Oleic Acid
Zdroj: Toxicology mechanisms and methods. 27(4)
ISSN: 1537-6524
Popis: Diethylhexyl phthalate (DEHP) is suspected to be an inevitable factor related to metabolic disease. Our previous study demonstrated that excess DEHP could exacerbate non-alcoholic fatty liver disease (NAFLD) in SD rats. Addressing the terra incognita in DEHP-induced metabolic dysfunction, this study used HepG2 cells to investigate the potential mechanisms involved in DEHP-induced toxicity in vitro. The cells were established lipid overload model with oleic acid and BSA, then exposed to different concentrations (5, 10, 25, 50, 100 μmol/l DEHP) of DEHP for further analysis. The Oil Red O staining results showed that DEHP could promote lipid accumulation in cells. The level of superoxide dismutase (SOD) and malondialdehyde (MDA) changed suggested the balance of oxidative stress was disrupted. Additionally, western blot analysis showed that DEHP could promote the expression of peroxisome proliferator-activated receptor α (PPARα) and sterol regulatory element-binding protein 1c (SREBP-1c). By quantifying the expressions of the two proteins, it is of interest to determine that DEHP could promote lipid accumulation in hepatocytes via activating the SREBP-1c and PPARα-signaling pathway.
Databáze: OpenAIRE