Hepcidin in non-alcoholic fatty liver disease regulated by the TLR4/NF-κB signaling pathway

被引:22
|
作者
Chen, Wei [1 ]
Wang, Xiaowei [1 ]
Huang, Li [2 ]
Liu, Bo [1 ]
机构
[1] Hubei Univ Med, Xiangyang Hosp, Dept Gastroenterol, Xiangyang 441000, Hubei, Peoples R China
[2] Hubei Univ Med, Xiangyang Hosp, Dept Neurol, Xiangyang 441000, Hubei, Peoples R China
关键词
Hepcidin; non-alcoholic fatty liver disease; toll-like receptor 4; nuclear factor-kappa B; pathenolide; METABOLISM; IRON; BIOMARKERS; STATE; CELLS;
D O I
10.3892/etm.2015.2873
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The aim of our study was to analyze the role of toll-like receptor 4 (TLR4)/nuclear factor (NF)-kappa B 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 mu mol/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-kappa B in liver tissues were quantified by western blotting. NAFLD rats appeared to have typical liver fatty degeneration and the expression of TLR4/NF-kappa B 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-kappa B protein and Hepcidin mRNA expression (P<0.05). In conclusion, the abnormal activation of the TLR4/NF-kappa B signaling pathway may cause NAFLD through the overexpression of Hepcidin.
引用
收藏
页码:73 / 76
页数:4
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