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Updated: Jul 5, 2025

Murine Colitis Modeling using Dextran Sulfate Sodium DSS
08:39

Murine Colitis Modeling using Dextran Sulfate Sodium DSS

Published on: January 19, 2010

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Baricitinib relieves DSS-induced ulcerative colitis in mice by suppressing the NF-κB and JAK2/STAT3 signalling

Qiong Wu1,2, Yangyang Liu1,2, Jinmeiqi Liang1,2

  • 1Department of Immunology, School of Basic Medical Sciences, Hubei University of Medicine, 30 Renmin Road, Shiyan, 442000, Hubei, People's Republic of China.

Inflammopharmacology
|January 16, 2024
PubMed

Insights

Baricitinib, a Janus kinase (JAK) inhibitor, effectively reduced inflammation in a mouse model of ulcerative colitis (UC). This study suggests baricitinib as a potential new treatment for colitis.

Area of Science:

  • Gastroenterology
  • Immunology
  • Pharmacology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory condition with limited treatment options.
  • Baricitinib, a Janus kinase (JAK) inhibitor, is approved for rheumatoid arthritis but its efficacy in UC is not well-established.
  • Developing novel therapeutics for UC is a critical unmet need.

Purpose of the Study:

  • To investigate the therapeutic potential of baricitinib in a dextran sulphate sodium (DSS)-induced mouse model of chronic colitis.
  • To elucidate the underlying molecular mechanisms of baricitinib's action in colitis.
  • To evaluate the impact of baricitinib on key inflammatory cytokines and signaling pathways.

Main Methods:

  • Oral administration of baricitinib to mice with DSS-induced colitis.
  • Measurement of pro-inflammatory cytokine levels (IL-6, IFN-γ, IL-17A) in vitro and in vivo.
  • Western blotting analysis to assess the expression of proteins involved in the JAK/STAT pathway (IκBα, p-IκBα, JAK2, p-JAK2, STAT3, p-STAT3).

Main Results:

  • Baricitinib significantly alleviated the symptoms of DSS-induced colitis in mice.
  • Treatment with baricitinib led to decreased levels of IL-6, IFN-γ, and IL-17A.
  • Baricitinib intervention reduced the elevated expression of phosphorylated IκBα, JAK2, and STAT3, indicating modulation of the JAK/STAT pathway.

Conclusions:

  • Baricitinib demonstrates significant therapeutic efficacy in a preclinical model of ulcerative colitis.
  • The anti-inflammatory effects of baricitinib in colitis are mediated through the inhibition of key inflammatory cytokines and the JAK/STAT signaling pathway.
  • Baricitinib represents a promising candidate for further clinical investigation as a treatment for ulcerative colitis.
Keywords:
BaricitinibJAK2/STAT3NF-κBPro-inflammatory cytokinesUlcerative colitis (UC)

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