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

Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

1.7K
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
1.7K
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

1.5K
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
1.5K
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

1.5K
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
1.5K
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

1.5K
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
1.5K
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

1.0K
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
1.0K
Gastritis III: Clinical Manifestations and Management01:23

Gastritis III: Clinical Manifestations and Management

1.7K
The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
1.7K

You might also read

Related Articles

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

Sort by
Same author

Healthy Aging Biomarkers: The INSPIRE's Contribution.

The Journal of frailty & aging·2021
Same author

The INSPIRE Research Initiative: A Program for GeroScience and Healthy Aging Research Going from Animal Models to Humans and the Healthcare System.

The Journal of frailty & aging·2021
Same author

The INSPIRE Bio-Resource Research Platform for Healthy Aging and Geroscience: Focus on the Human Translational Research Cohort (The INSPIRE-T Cohort).

The Journal of frailty & aging·2021
Same author

Towards a Large-Scale Assessment of the Relationship between Biological and Chronological Aging: The INSPIRE Mouse Cohort.

The Journal of frailty & aging·2021
Same author

Revisiting the Hallmarks of Aging to Identify Markers of Biological Age.

The journal of prevention of Alzheimer's disease·2020
Same author

[TRENDS IN DEVELOPMENT OF GI-SAFE ANTI-INFLAMMATORY DRUGS].

Klinicheskaia meditsina·2018

Related Experiment Video

Updated: Mar 31, 2026

Author Spotlight: Developing a Rat Model for Pouchitis Research and Treatment
04:05

Author Spotlight: Developing a Rat Model for Pouchitis Research and Treatment

Published on: May 31, 2024

1.0K

NSAID-induced gastric damage in rats: requirement for inhibition of both cyclooxygenase 1 and 2.

J L Wallace1, W McKnight, B K Reuter

  • 1Mucosal Inflammation Research Group, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada. wallacej@ucalgary.ca

Gastroenterology
|September 13, 2000
PubMed
Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause gastric injury by inhibiting both cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). Selective COX-1 or COX-2 inhibition alone does not cause damage, but combined inhibition invariably leads to gastric erosions in rats.

More Related Videos

Synthesis of a Borylated Ibuprofen Derivative Through Suzuki Cross-Coupling and Alkene Boracarboxylation Reactions
08:56

Synthesis of a Borylated Ibuprofen Derivative Through Suzuki Cross-Coupling and Alkene Boracarboxylation Reactions

Published on: November 30, 2022

3.6K
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

4.7K

Related Experiment Videos

Last Updated: Mar 31, 2026

Author Spotlight: Developing a Rat Model for Pouchitis Research and Treatment
04:05

Author Spotlight: Developing a Rat Model for Pouchitis Research and Treatment

Published on: May 31, 2024

1.0K
Synthesis of a Borylated Ibuprofen Derivative Through Suzuki Cross-Coupling and Alkene Boracarboxylation Reactions
08:56

Synthesis of a Borylated Ibuprofen Derivative Through Suzuki Cross-Coupling and Alkene Boracarboxylation Reactions

Published on: November 30, 2022

3.6K
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

4.7K

Area of Science:

  • Gastroenterology
  • Pharmacology
  • Biochemistry

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to cause gastric damage.
  • Selective cyclooxygenase-2 (COX-2) inhibitors cause less gastric damage than conventional NSAIDs, suggesting COX-1 inhibition mediates gastric injury.
  • This study investigated the role of COX-1 inhibition in NSAID-induced gastric damage.

Purpose of the Study:

  • To test the hypothesis that cyclooxygenase-1 (COX-1) inhibition is responsible for nonsteroidal anti-inflammatory drug (NSAID)-induced gastric damage.
  • To evaluate the effects of selective COX-1 and COX-2 inhibitors, alone and in combination, on gastric integrity in rats.

Main Methods:

  • Administered selective COX-1 inhibitor (SC-560) and selective COX-2 inhibitor (celecoxib) to rats.
  • Assessed gastric damage, prostaglandin synthesis, leukocyte adherence, and gastric blood flow.
  • Determined drug selectivity for COX-1 versus COX-2 using the carrageenan-airpouch model.

Main Results:

  • Selective COX-1 inhibition (SC-560) reduced prostaglandin synthesis but did not cause gastric damage.
  • Selective COX-2 inhibition (celecoxib) did not affect prostaglandin E(2) synthesis or cause gastric damage.
  • Combination of SC-560 and celecoxib invariably caused significant hemorrhagic gastric erosion, similar to indomethacin.

Conclusions:

  • Nonsteroidal anti-inflammatory drug (NSAID)-induced gastric injury in rats requires the inhibition of both cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2).
  • Selective inhibition of either COX isoform alone is insufficient to cause significant gastric damage.