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Decoy receptor 3 alleviates hepatic fibrosis through suppressing inflammation activated by NF-κB signaling pathway

Zhenjing Jin1, Siqi Liu1, Qian Zhan1

  • 1The Second Clinical Hospital, Jilin University, Changchun, China

Advances in Clinical and Experimental Medicine : Official Organ Wroclaw Medical University
|March 21, 2018
PubMed
Abstract

Insights

Decoy receptor 3 (DcR3) effectively reduced liver injury and inflammation in rats with hepatic fibrosis. This suggests DcR3 shows promise as a potential prophylactic and therapeutic agent for treating liver fibrosis.

Area of Science:

  • Hepatology
  • Immunology
  • Biomedical Research

Background:

  • Hepatic fibrosis is a pathological process characterized by inflammation.
  • Decoy receptor 3 (DcR3) exhibits anti-inflammatory properties.

Purpose of the Study:

  • To investigate the potential preventive effects of DcR3 on hepatic fibrosis.
  • To evaluate DcR3 as a therapeutic agent for liver fibrosis.

Main Methods:

  • Hepatic fibrosis induced in rats using dimethylnitrosamine (DMN).
  • DcR3 plasmid delivered via intravenous injection.
  • Analysis of liver tissue for DcR3, TL1A, α-SMA, inflammatory cytokines (TNF-α, IL-6, IL-1β), and NF-κB activation.

Main Results:

  • DcR3 treatment significantly increased DcR3 expression in rat livers.
  • DcR3 administration attenuated liver pathology and reduced α-SMA, TL1A, TNF-α, IL-6, and IL-1β levels.
  • DcR3 inhibited NF-κB activation in the liver tissue.

Conclusions:

  • DcR3 demonstrates efficacy in attenuating liver injury and inflammatory responses in a rat model of hepatic fibrosis.
  • DcR3 is a promising prophylactic and therapeutic candidate for hepatic fibrosis treatment.
Keywords:
NF-κBTNF-like molecule 1Adecoy receptor 3hepatic fibrosisinflammatory response

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