Gastroprotective Mechanisms in Ulcerative Disorders
Summary
Ulcerative disorders of the upper gastrointestinal tract result from an imbalance between mucosal aggressive factors—such as gastric acid, pepsin and Helicobacter pylori—and intrinsic defence mechanisms. Effective gastroprotection depends on acid suppression to reduce mucosal injury, alongside enhancement of the epithelial barrier through increased mucus and bicarbonate secretion. Cytoprotective mediators, notably prostaglandins and nitric oxide, improve mucosal blood flow, stimulate mucus production and inhibit neutrophil adhesion. Antioxidant systems neutralise reactive oxygen species generated during inflammation, thereby limiting lipid peroxidation and apoptosis. Anti-inflammatory pathways modulate cytokine release to curb neutrophil infiltration and oxidative burst. In parallel, tissue repair processes including epithelial restitution and angiogenesis, supported by growth factors, restore mucosal integrity. Emerging research highlights the role of host–microbe interactions and modulation of the microbiota in fortifying mucosal immunity. Together, these coordinated mechanisms form the basis for current therapies and suggest novel targets for preventing ulcer formation and promoting healing on a global scale.
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Gastroprotective Mechanisms in Ulcerative Disorders publication trend
The graph below shows the total number of articles in gastroprotective mechanisms in ulcerative disorders across all publications each year (not limited to Nature Index journals).
Technical terms
Cytoprotection: Strengthening of mucosal defence mechanisms to prevent injury despite ongoing exposure to aggressive factors.
Mucus gel layer: A protective film of mucus and bicarbonate that coats the epithelium, buffering acid and preventing erosion.
Prostaglandins: Lipid mediators that enhance mucosal blood flow, stimulate mucus and bicarbonate secretion, and inhibit acid secretion.
Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen that can damage cellular lipids, proteins and DNA.
Proton pump inhibitors (PPIs): Drugs that irreversibly inhibit the gastric H+/K+-ATPase enzyme in parietal cells, markedly reducing acid secretion.
Histamine-2 receptor antagonists (H2RAs): Medications that block H2 receptors on parietal cells to diminish gastric acid output.
References
- Effects of gastroprotectant drugs for the prevention and treatment of peptic ulcer disease and its complications: a meta-analysis of randomised trials. The Lancet Gastroenterology & Hepatology (2018).
- Antiulcer Agents: From Plant Extracts to Phytochemicals in Healing Promotion. Molecules (2018).
- The global, regional and national burden of peptic ulcer disease from 1990 to 2019: a population-based study. BMC Gastroenterology (2022).
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