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Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.

Gastritis-II: Pathophysiology

Gastritis-II: Pathophysiology

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...

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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. Bicarbonate,...

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

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

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...

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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 to M3...

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Updated: May 25, 2026

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Published on: May 5, 2022

NSAIDs and acidic environment induce gastric mucosal cellular mitochondrial dysfunction.

Yumiko Nagano¹, Hirofumi Matsui, Masato Tamura

¹The Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, Japan.

|January 25, 2012

Summary

Non-steroidal anti-inflammatory drugs (NSAIDs) and gastric acid synergistically damage stomach cells. This combined effect increases mitochondrial superoxide production, leading to gastric epithelial injury and potential ulcers.

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Last Updated: May 25, 2026

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Published on: May 5, 2022

Area of Science:

Gastroenterology
Cell Biology
Pharmacology

Background:

Non-steroidal anti-inflammatory drugs (NSAIDs) are common causes of gastrointestinal issues like ulcers.
NSAIDs induce lipid peroxidation in gastric cells via mitochondrial superoxide, independent of prostaglandin deficiency.
Gastric acid (HCl) is increasingly recognized as a factor in gastric mucosal injuries, inducing lipid peroxidation in vitro.

Purpose of the Study:

To investigate the synergistic effects of gastric acid and NSAIDs on gastric epithelial cells.
To determine if combined acid and NSAID treatment enhances cellular injury and mitochondrial superoxide production.

Main Methods:

RGM1 gastric epithelial cells were pretreated with acidic solutions.
Cells were subsequently treated with various NSAIDs.
Cellular injury, lipid peroxidation, mitochondrial membrane potential, and mitochondrial superoxide levels were assessed.

Main Results:

Exposure to both acid and NSAIDs induced significant cellular injury in RGM1 cells.
The combined treatment led to increased lipid peroxidation and mitochondrial superoxide production.
Evidence suggests a synergistic interaction between gastric acid and NSAIDs in damaging gastric cells.

Conclusions:

Gastric acid and NSAIDs act synergistically to induce cellular injury in gastric epithelial cells.
This synergistic effect is mediated, at least in part, by increased mitochondrial superoxide production.
Understanding this interaction is crucial for preventing NSAID-induced gastrointestinal complications.