Related Experiment Video

Updated: Jun 2, 2026

Evaluation of the Efficacy of the H. pylori Protein HP-NAP as a Therapeutic Tool for Treatment of Bladder Cancer in an Orthotopic Murine Model
06:12

Evaluation of the Efficacy of the H. pylori Protein HP-NAP as a Therapeutic Tool for Treatment of Bladder Cancer in an Orthotopic Murine Model

Published on: May 29, 2015

[Gastroprotective action of the nettle extract in experimental peptic ulcer]

V N Burkova, S G Boev, A I Vengerovskiĭ

    Eksperimental'Naia I Klinicheskaia Farmakologiia
    |April 12, 2011
    PubMed

    Related Concept Videos

    Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

    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...
    Peptic Ulcer Disease IV: Management01:26

    Peptic Ulcer Disease IV: Management

    Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
    The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
    Pharmacological management
    The prevailing therapy for peptic ulcers involves a combination of managing the patient's current medication...
    Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

    Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

    In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
    In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
    Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

    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,...
    Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

    Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

    Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
    Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
    Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

    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...