Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Inflammatory Bowel Disease I: Introduction01:26

Inflammatory Bowel Disease I: Introduction

Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows “skip lesions” in which...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effect of quarterly meeting and email report of ADR, cecal intubation rate, and withdrawal time on personal and group quality measures in colonoscopy.

Revista de gastroenterologia de Mexico (English)·2025
Same author

The impact of the COVID-19 pandemic on UK medical education. A nationwide student survey.

Medical teacher·2021
Same author

Basic symptoms influence real-life functioning and symptoms in individuals at high risk for psychosis.

Acta psychiatrica Scandinavica·2019
Same author

Intranasal fentanyl and inhaled nitrous oxide for fracture reduction: The FAN observational study.

The American journal of emergency medicine·2017
Same author

Generation and evaluation of typical meteorological year datasets for greenhouse and external conditions on the Mediterranean coast.

International journal of biometeorology·2014
Same author

Biofeedback-assisted relaxation in insulin-dependent diabetes: A replication and extension study.

Annals of behavioral medicine : a publication of the Society of Behavioral Medicine·2013
Same journal

Association of C-Reactive Protein-Triglyceride Glucose Index With Chronic Obstructive Pulmonary Disease: Results From the NHANES and CHARLS Cohorts.

Mediators of inflammation·2026
Same journal

Moxibustion Modulates ALOX15-Mediated Lipid Peroxidation to Inhibit Ferroptosis in Synovial Inflammatory Injury of Rheumatoid Arthritis.

Mediators of inflammation·2026
Same journal

Development and Validation of a Cytokine-Based Predictive Model for Acute GvHD and Composite Outcomes in ATG-Based Haploidentical Hematopoietic Stem Cell Transplantation.

Mediators of inflammation·2026
Same journal

Effects of Livergol and Hydroalcoholic Extracts of Barberry, Jujube, and Flixweed on Oxidative Stress and Inflammatory Gene Expression in a MASLD Animal Model.

Mediators of inflammation·2026
Same journal

Immune Gene INHBA is Associated With Osteoarthritic Cartilage Damage and May Mediate the Temporal Activation of the TGF-β/p38 MAPK Pathway: Integrating Multiomics Machine Learning and Experimental Validation.

Mediators of inflammation·2026
Same journal

RETRACTION: IκB Kinase Inhibitor VII Modulates Sepsis-Induced Excessive Inflammation and Cardiac Dysfunction in 5/6 Nephrectomized Mice.

Mediators of inflammation·2026
See all related articles

Related Experiment Video

Updated: Jul 5, 2026

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

Stress induced experimental colitis.

T A Stein1, L Keegan, L J Auguste

  • 1Department of Surgery Long Island Jewish Medical Center The Long Island Campus for the Albert Einstein College of Medicine 270-05 76th Avenue New Hyde Park NY 11042 USA.

Mediators of Inflammation
|January 1, 1993
PubMed
Summary
This summary is machine-generated.

Stress significantly increases prostaglandin E(2) and leukotriene C(4) synthesis in the rat colon, leading to mucosal damage. These findings suggest a link between stress, inflammation, and digestive tract health.

More Related Videos

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease
05:08

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease

Published on: March 1, 2022

Investigating Intestinal Inflammation in DSS-induced Model of IBD
08:43

Investigating Intestinal Inflammation in DSS-induced Model of IBD

Published on: February 1, 2012

Related Experiment Videos

Last Updated: Jul 5, 2026

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease
05:08

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease

Published on: March 1, 2022

Investigating Intestinal Inflammation in DSS-induced Model of IBD
08:43

Investigating Intestinal Inflammation in DSS-induced Model of IBD

Published on: February 1, 2012

Area of Science:

  • Gastroenterology
  • Neuroscience
  • Biochemistry

Background:

  • Stress impacts the central nervous system, altering digestive tract physiology.
  • Understanding stress-induced colonic changes is crucial for digestive health.

Purpose of the Study:

  • To investigate arachidonic acid oxidation and colonic damage following stress.
  • To quantify changes in prostaglandin E(2) and leukotriene C(4) synthesis in response to stress.

Main Methods:

  • Cold-restraint stress applied to rats.
  • Assessment of colonic mucosal erosions and hemorrhage.
  • Measurement of prostaglandin E(2) and leukotriene C(4) synthesis.

Main Results:

  • Stress induced mucosal erosions and subepithelial hemorrhage in the proximal colon.
  • Prostaglandin E(2) synthesis increased significantly post-stress (1610 vs. 381 ng/g/min).
  • Leukotriene C(4) synthesis also elevated significantly post-stress (11300 vs. 4217 ng/g/min).
  • Prostaglandin E(2) synthesis correlated positively with leukotriene C(4) synthesis (r=0.9381).

Conclusions:

  • Stress causes significant biochemical and pathological changes in the rat colon.
  • Increased prostaglandin and leukotriene synthesis are key components of the colonic stress response.
  • The colonic response to stress may be less severe than gastric response due to regional regulatory mechanisms.