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

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...
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...
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
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,...
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...

You might also read

Related Articles

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

Sort by
Same author

Results of Surgical Treatment of Carcinoma of the Penis.

The Australian and New Zealand journal of surgeryยท2017
Same author

Results of surgical treatment of carcinoma of the penis.

The Australian and New Zealand journal of surgeryยท1971
See all related articles

Related Experiment Video

Updated: May 12, 2026

Qualitative and Quantitative Assays for Detection and Characterization of Protein Antimicrobials
10:50

Qualitative and Quantitative Assays for Detection and Characterization of Protein Antimicrobials

Published on: April 10, 2016

Antipeptic activity of antacids.

J T Kuruvilla

    Gut
    |November 1, 1971
    PubMed
    Summary

    This study investigated antacid preparations, finding no evidence that they possess intrinsic antipeptic activity beyond altering pH. Claims of inherent pepsin inhibition by antacids were not supported by in vitro experiments.

    Area of Science:

    • Gastroenterology
    • Pharmacology
    • Biochemistry

    Background:

    • Antacids are widely used to manage acid-related gastrointestinal disorders.
    • Some antacid manufacturers claim their products have intrinsic antipeptic activity.
    • This activity is purported to be independent of pH alteration.

    Purpose of the Study:

    • To experimentally evaluate the claimed intrinsic antipeptic activity of commercial antacids.
    • To determine if antacids inhibit pepsin directly, irrespective of pH changes.

    Main Methods:

    • An in vitro digestion model using haemoglobin as a substrate was employed.
    • The effect of various antacids on pepsin activity was assessed.
    • Experiments were conducted to differentiate direct antipeptic effects from pH-mediated effects.

    More Related Videos

    One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
    10:44

    One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

    Published on: June 18, 2016

    Expression, Purification, and Antimicrobial Activity of S100A12
    11:10

    Expression, Purification, and Antimicrobial Activity of S100A12

    Published on: May 13, 2017

    Related Experiment Videos

    Last Updated: May 12, 2026

    Qualitative and Quantitative Assays for Detection and Characterization of Protein Antimicrobials
    10:50

    Qualitative and Quantitative Assays for Detection and Characterization of Protein Antimicrobials

    Published on: April 10, 2016

    One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
    10:44

    One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

    Published on: June 18, 2016

    Expression, Purification, and Antimicrobial Activity of S100A12
    11:10

    Expression, Purification, and Antimicrobial Activity of S100A12

    Published on: May 13, 2017

    Main Results:

    • In vitro experiments did not substantiate claims of intrinsic antipeptic activity for the tested antacids.
    • No direct inhibition of pepsin by the antacids was observed independent of pH modification.
    • Observed effects on haemoglobin digestion were attributable to pH changes induced by the antacids.

    Conclusions:

    • The intrinsic antipeptic activity claimed by some antacid manufacturers could not be verified.
    • The primary mechanism by which these antacids affect pepsin appears to be through altering the local pH environment.
    • Further research may be needed to clarify the precise mechanisms of action for all antacid formulations.