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. 2016 Jan;11(1):73-76.
doi: 10.3892/etm.2015.2873. Epub 2015 Nov 17.

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

Wei Chen  1 , Xiaowei Wang  1 , L I Huang  2 , B O Liu  1
Affiliations

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

Wei Chen et al. Exp Ther Med. 2016 Jan.

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.

Keywords: Hepcidin; non-alcoholic fatty liver disease; nuclear factor-κB; pathenolide; toll-like receptor 4.

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Figures

Figure 1.
Figure 1.
Histological analysis of liver biopsy. (A) Control, (B) non-alcoholic fatty liver disease and (C) intervention groups.
Figure 2.
Figure 2.
Western blot analysis of toll like receptor 4 (TLR4) and nuclear factor (NF)-κB. (1) Control, (2) non-alcoholic fatty liver disease and (3) intervention groups
Figure 3.
Figure 3.
Quantitative polymerase chain reaction examination of Hepcidin mRNA of (1) control, (2) non-alcoholic fatty liver disease and (3) intervention groups. (M) 100 bp marker.
See this image and copyright information in PMC

References

    1. Rinella ME. Nonalcoholic fatty liver disease: a systematic review. JAMA. 2015;313:2263–2273. doi: 10.1001/jama.2015.5370. - DOI - PubMed
    1. Targher G, Chonchol MB, Byrne CD. CKD and nonalcoholic fatty liver disease. Am J Kidney Dis. 2014;64:638–652. doi: 10.1053/j.ajkd.2014.05.019. - DOI - PubMed
    1. Granér M, Nyman K, Siren R, Pentikäinen MO, Lundbom J, Hakkarainen A, Lauerma K, Lundbom N, Nieminen MS, Taskinen MR. Ectopic fat depots and left ventricular function in nondiabetic men with nonalcoholic fatty liver disease. Circ Cardiovasc Imaging. 2015;8:e001979. doi: 10.1161/CIRCIMAGING.114.001979. - DOI - PubMed
    1. Fargion S, Porzio M, Fracanzani AL. Nonalcoholic fatty liver disease and vascular disease: state-of-the-art. World J Gastroenterol. 2014;20:13306–13324. doi: 10.3748/wjg.v20.i37.13306. - DOI - PMC - PubMed
    1. Wu H, Jin M, Han D, Zhou M, Mei X, Guan Y, Liu C. Protective effects of aerobic swimming training on high-fat diet induced nonalcoholic fatty liver disease: Regulation of lipid metabolism via PANDER-AKT pathway. Biochem Biophys Res Commun. 2015;458:862–868. doi: 10.1016/j.bbrc.2015.02.046. - DOI - PubMed

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