Inhibition of CCL19 benefits non‑alcoholic fatty liver disease by inhibiting TLR4/NF‑κB‑p65 signaling

  • Authors:
    • Jiajing Zhao
    • Yingjue Wang
    • Xi Wu
    • Ping Tong
    • Yaohan Yue
    • Shurong Gao
    • Dongping Huang
    • Jianwei Huang
  • View Affiliations

  • Published online on: September 14, 2018     https://doi.org/10.3892/mmr.2018.9490
  • Pages: 4635-4642
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Non‑alcoholic fatty liver disease (NAFLD), which affects approximately one‑third of the general population, has become a global health problem. Thus, more effective treatments for NAFLD are urgently required. In the present study, high levels of C‑C motif ligand 19 (CCL19), signaling pathways such as Toll‑like receptor 4 (TLR4)/nuclear factor‑κB (NF‑κB), and proinflammatory factors including interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) were detected in NAFLD patients, thereby indicating that there may be an association between CCL19 and these factors in NAFLD progression. Using a high‑fat diet (HFD), the present study generated a Sprague‑Dawley rat model of NAFLD, which displayed dyslipidemia with increased levels of plasma aspartate aminotransferase, alanine aminotransferase, total cholesterol and triglyceride. Dyslipidemia, liver histopathology and gene expression analyses indicated that the NAFLD model was successfully induced by HFD, and metformin and berberine (BBR) were effective treatments for NAFLD. HFD‑induced CCL19 levels and associated factors were markedly reduced by the two drug treatments. In addition, metformin or BBR alone significantly promoted adenosine monophosphate‑activated protein kinase (AMPK) phosphorylation, which was inhibited by HFD. These results demonstrated that metformin and BBR could improve NAFLD, which may be via the activation of AMPK signaling, and the high expression of CCL19 in NAFLD was significantly reduced by metformin and BBR. It could be inferred that inhibition of CCL19 may be an effective treatment for NAFLD.
View Figures
View References

Related Articles

Journal Cover

November-2018
Volume 18 Issue 5

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhao J, Wang Y, Wu X, Tong P, Yue Y, Gao S, Huang D and Huang J: Inhibition of CCL19 benefits non‑alcoholic fatty liver disease by inhibiting TLR4/NF‑κB‑p65 signaling. Mol Med Rep 18: 4635-4642, 2018
APA
Zhao, J., Wang, Y., Wu, X., Tong, P., Yue, Y., Gao, S. ... Huang, J. (2018). Inhibition of CCL19 benefits non‑alcoholic fatty liver disease by inhibiting TLR4/NF‑κB‑p65 signaling. Molecular Medicine Reports, 18, 4635-4642. https://doi.org/10.3892/mmr.2018.9490
MLA
Zhao, J., Wang, Y., Wu, X., Tong, P., Yue, Y., Gao, S., Huang, D., Huang, J."Inhibition of CCL19 benefits non‑alcoholic fatty liver disease by inhibiting TLR4/NF‑κB‑p65 signaling". Molecular Medicine Reports 18.5 (2018): 4635-4642.
Chicago
Zhao, J., Wang, Y., Wu, X., Tong, P., Yue, Y., Gao, S., Huang, D., Huang, J."Inhibition of CCL19 benefits non‑alcoholic fatty liver disease by inhibiting TLR4/NF‑κB‑p65 signaling". Molecular Medicine Reports 18, no. 5 (2018): 4635-4642. https://doi.org/10.3892/mmr.2018.9490