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Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice
Published on: March 10, 2017
Hepcidin in non-alcoholic fatty liver disease regulated by the TLR4/NF-κB signaling pathway
Wei Chen1, Xiaowei Wang1, L I Huang2
1Department of Gastroenterology, Xiangyang Hospital Affiliated to Hubei University of Medicine, Xiangyang, Hubei 441000, P.R China.
Abstract:
The aim of our study was to analyze the role of toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB signal pathway on Hepcidin regulation in non-alcoholic fatty liver disease (NAFLD). A total of 60 male Sprague-Dawley rats were randomly divided into the control, NAFLD and intervention groups. Rats in the control group were fed with standard laboratory diet, and rats in the NAFLD and intervention groups were fed with a high-fat diet. A final volume of 2 ml of pathenolide (10 µmol/l) was administered intraperitoneally only to the rats in the intervention group. The tissue sections were stained with hematoxylin and eosin and the pathological changes in liver tissues were observed and scored. The levels of TLR4 and NF-κB in liver tissues were quantified by western blotting. NAFLD rats appeared to have typical liver fatty degeneration and the expression of TLR4/NF-κB proteins and Hepcidin mRNA was significantly higher than that in the control group (P<0.05). However, the pathological changes observed in the intervention group had a marked improvement with a significant reduction in the TLR4/NF-κB protein and Hepcidin mRNA expression (P<0.05). In conclusion, the abnormal activation of the TLR4/NF-κB signaling pathway may cause NAFLD through the overexpression of Hepcidin.
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