| Literature DB >> 31264285 |
Huiyan Zhang1,2, Jicang Wang3, Ling Yang1,2, Wenling Yang1,2, Tongwang Luo1,2, Yan Yuan1,2, Jianhong Gu1,2, Hui Zou1,2, Jianchun Bian1,2, Zongping Liu1,2, Xuezhong Liu1,2.
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.Entities:
Keywords: BRL 3A; apoptosis; lipotoxicity; oleic acid; oxidative stress
Year: 2019 PMID: 31264285 DOI: 10.1002/jcb.29262
Source DB: PubMed Journal: J Cell Biochem ISSN: 0730-2312 Impact factor: 4.429