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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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Deoxyschizandrin treats mice with ulcerative colitis possibly via the TLR4/NF-κB signaling pathway

Sheng Yu1, Haihua Qian2

  • 1Surgery of Traditional Chinese Medicine, Nanjing University of Traditional Chinese Medicine, The First Clinical Medical College Nanjing 210000, Jiangsu Province, China.

American Journal of Translational Research
|May 21, 2021
PubMed
Abstract

Insights

Deoxyschizandrin (DSD) effectively treats ulcerative colitis (UC) in mice by reducing inflammation and cell damage. DSD works by inhibiting the TLR4/NF-κB signaling pathway, offering a potential new therapy for UC.

Area of Science:

  • Pharmacology
  • Gastroenterology
  • Immunology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease with limited treatment options.
  • Understanding the molecular mechanisms underlying UC is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the therapeutic effects of deoxyschizandrin (DSD) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in a mouse model.
  • To elucidate the underlying mechanisms by which DSD exerts its protective effects in UC.

Main Methods:

  • Establishment of UC mouse models using DSS administration.
  • Treatment of UC mice with deoxyschizandrin (DSD).
  • Evaluation of therapeutic efficacy through clinical observations and molecular analysis of colonic tissues.

Main Results:

  • DSS-induced UC mice exhibited increased disease activity, inflammation, oxidative stress, and colonic epithelial cell apoptosis.
  • DSD treatment significantly ameliorated these UC symptoms.
  • DSD intervention reduced the elevated levels of TLR4, MyD88, and NF-κB in the colonic tissues of UC mice.

Conclusions:

  • Deoxyschizandrin (DSD) demonstrates significant therapeutic potential for ulcerative colitis (UC).
  • DSD alleviates UC symptoms by inhibiting inflammation, oxidative stress, and apoptosis.
  • The protective effects of DSD are likely mediated through the inhibition of the TLR4/NF-κB signaling pathway.
Keywords:
DeoxyschizandrinTLR4/NF-κBmiceulcerative colitis

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