Related Experiment Video

Updated: Mar 30, 2026

Chronic Salmonella Infection Induced Intestinal Fibrosis
08:40

Chronic Salmonella Infection Induced Intestinal Fibrosis

Published on: September 22, 2019

7.7K

Novel PPARγ Modulator GED-0507-34 Levo Ameliorates Inflammation-driven Intestinal Fibrosis

Silvia Speca1, Christel Rousseaux, Caroline Dubuquoy

  • 1*Inserm, LIRIC UMR995, Lille, France; †CHRU de Lille, Service des Maladies de l'Appareil Digestif et de la Nutrition, Hôpital Claude Huriez, LIRIC, UMR995, Lille, France; ‡Department of Life, Health and Environmental Sciences, Gastroenterology Unit, University of L'Aquila, L'Aquila, Italy; §IBD, Lille, France; ‖Department of Pathobiology, Lerner Research Institute, and Department of Gastroenterology, Hepatology & Nutrition, Digestive Disease Institute, Cleveland Clinic Foundation, Cleveland, Ohio; ¶Université Lille Nord de France, Lille, France; and **Department of Human Anatomy, University of Roma "La Sapienza," Roma, Italy.

Inflammatory Bowel Diseases
|November 5, 2015
PubMed
Abstract

Insights

This study shows GED, a novel 5-ASA analog, effectively reduces intestinal fibrosis in mice by targeting key profibrotic pathways. GED offers a potential new therapeutic strategy for fibrotic conditions like Crohn's disease.

Area of Science:

  • Gastroenterology
  • Pharmacology
  • Fibrosis Research

Background:

  • Intestinal fibrosis, characterized by excessive extracellular matrix deposition, is a major complication of Crohn's disease.
  • Currently, no specific antifibrotic therapies are available for intestinal fibrosis.
  • This study investigates the antifibrotic potential of GED-0507-34 Levo, a novel 5-ASA analog activating peroxisome proliferator-activated receptor γ.

Purpose of the Study:

  • To evaluate the antifibrotic effects of GED in a mouse model of colonic fibrosis.
  • To determine the impact of GED on myofibroblast activation markers and profibrotic signaling pathways.
  • To assess GED's efficacy in human intestinal fibroblasts from ulcerative colitis patients.

Main Methods:

  • Colonic fibrosis was induced in mice using dextran sulfate sodium (DSS).
  • Preventive effects of oral GED administration were assessed via macroscopic and histological scores, alongside biological endpoints.
  • The expression of myofibroblast activation markers and TGF-β pathway components was analyzed in stimulated intestinal cells and patient-derived fibroblasts.

Main Results:

  • GED significantly improved intestinal lesions and reduced profibrotic gene expression (Acta2, COL1a1, Fn1) in DSS-treated mice.
  • GED decreased protein levels of fibrosis markers (α-SMA, Collagen I-II) and TGF-β/Smad pathway components.
  • GED inhibited TGF-β-induced activation in fibroblast and epithelial cells, and reduced TGF-β and ACTA1 expression in human ulcerative colitis fibroblasts.

Conclusions:

  • GED demonstrates significant amelioration of intestinal fibrosis in a DSS-induced chronic colitis mouse model.
  • GED effectively regulates key cellular and molecular mechanisms underlying intestinal fibrosis.
  • The findings suggest GED as a promising therapeutic agent for intestinal fibrosis.

More Related Videos

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

7.9K
Functional Assessment of Intestinal Permeability and Neutrophil Transepithelial Migration in Mice using a Standardized Intestinal Loop Model09:24

Functional Assessment of Intestinal Permeability and Neutrophil Transepithelial Migration in Mice using a Standardized Intestinal Loop Model

Published on: February 11, 2021

8.3K

Related Concept Videos

Inflammatory Bowel Disease IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
940
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
669
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by...
1.5K