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  2. Effect of oleic acid on induction of steatosis and cytotoxicity in BRL 3A cells

Effect of oleic acid on induction of steatosis and cytotoxicity in BRL 3A cells

  • J Cell Biochem. 2019 Dec;120(12):19541-19554. doi: 10.1002/jcb.29262.
Huiyan Zhang 1 2 Jicang Wang 3 Ling Yang 1 2 Wenling Yang 1 2 Tongwang Luo 1 2 Yan Yuan 1 2 Jianhong Gu 1 2 Hui Zou 1 2 Jianchun Bian 1 2 Zongping Liu 1 2 Xuezhong Liu 1 2
Affiliations

Affiliations

  • 1 College of Veterinary Medicine, Jiangsu Key Laboratory of Zoonosis, Yangzhou University, Yangzhou, Jiangsu, China.
  • 2 Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu, China.
  • 3 College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan, China.
Abstract

Recent studies have shown that monounsaturated oleic acid induces steatosis in cultured hepatocyte steatosis in the form of nonalcoholic fatty liver disease models in vitro. However, the underlying mechanism of steatosis development is not completely understood. Therefore, we investigated the molecular mechanism of steatosis and the role of mitogen-activated protein kinase (MAPK)/Toll-like Receptor 4-related protein (TLR4) expression in this study. Rat hepatocyte cells were subjected to oleic acid in different concentrations (1.2-2.4 mM) for 24 hours. The cell morphological injury index and the changes in the MAPK/TLR4 signaling pathway-related proteins were evaluated. We found that the microstructure of the cells in the oleic acid treatment group was damaged, and higher phosphorylation levels of the MAPK pathway-related proteins were detected than those in the control group. In addition, the protein expression of TLR4, sterol regulatory element-binding protein-1, and fatty acid synthase were increased in the oleic acid treatment group. Our findings demonstrate that oleic acid causes toxic damage to rat hepatocyte cells, and the MAPK/TLR4 signaling pathway plays a significant role in lipid storage.

Keywords

BRL 3A; apoptosis; lipotoxicity; oleic acid; oxidative stress.

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