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

Sympathetic Signaling01:31

Sympathetic Signaling

Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...
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...
Combined Effects of Drugs: Antagonism01:30

Combined Effects of Drugs: Antagonism

The combined effects of drugs can result in various interactions, of which an important type is antagonism. Antagonism is a mechanism where one drug inhibits or counteracts the effects of another drug. Antagonism can occur through various means, including receptor binding, allosteric modulation, functional interaction, chemical reactions, and pharmacokinetic processes.
The most common type is receptor antagonism, where one drug acts as an antagonist to block the effects of another drug by...
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: 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...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...

You might also read

Related Articles

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

Sort by
Same author

Orthostatic Hypotension in Hypertensive Patients Hospitalized in Italian Internal Medicine Departments: FADOI-HYP-OP Study.

High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension·2026
Same author

Pregnancy as a Window for Hypertension and Cardiovascular Prevention in Women: A Life-Course Perspective Based on the 2025 ESC Guidelines.

High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension·2026
Same author

Pain and its relationship with fatigue in Sjögren disease: an Italian single-centre experience.

EULAR rheumatology open·2026
Same author

Impact of anxiety and depression in patients with atrial fibrillation: Insights from 2 international prospective registries.

Heart rhythm·2026
Same author

Lipoprotein(a) and risk of dementia: A propensity score-matched real-world analysis from a global federated research network.

European journal of internal medicine·2026
Same author

Triglyceride-glucose index and its derived anthropometric indices: a comparative analysis for mortality prediction in the population cohort of the URRAH study.

Nutrition, metabolism, and cardiovascular diseases : NMCD·2026

Related Experiment Video

Updated: Jul 14, 2026

A Co-culture Method to Investigate the Crosstalk Between X-ray Irradiated Caco-2 Cells and PBMC
11:40

A Co-culture Method to Investigate the Crosstalk Between X-ray Irradiated Caco-2 Cells and PBMC

Published on: January 30, 2018

COX-2: friend or foe?

Annalisa Iezzi1, Claudio Ferri, Andrea Mezzetti

  • 1University of Chieti G.d'Annunzio, and the G.d'Annunzio University Foundation, Chieti, Italy.

Current Pharmaceutical Design
|June 23, 2007
PubMed
Summary

Cyclooxygenase-2 (COX-2) inhibitors offer therapeutic benefits for inflammation but carry risks of cardiovascular events. Understanding COX enzyme biology is crucial for developing safer anti-inflammatory treatments.

Area of Science:

  • Biochemistry and Pharmacology
  • Inflammation and Immunology
  • Cardiovascular Research

Background:

  • Two cyclooxygenase (COX) isoforms, COX-1 and COX-2, were hypothesized in 1990.
  • COX-1 maintains physiological functions (renal, gastric, platelet), while COX-2 is induced during inflammation.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) primarily target COX-2 for therapeutic effects.

Purpose of the Study:

  • To review the biology and pharmacology of cyclooxygenase enzymes.
  • To explore the role of COX enzymes in atherosclerosis.
  • To discuss the implications of selective COX-2 inhibition.

Main Methods:

  • Literature review of COX-1 and COX-2 biology and pharmacology.
  • Analysis of NSAID mechanisms and side effects.

More Related Videos

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

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

Related Experiment Videos

Last Updated: Jul 14, 2026

A Co-culture Method to Investigate the Crosstalk Between X-ray Irradiated Caco-2 Cells and PBMC
11:40

A Co-culture Method to Investigate the Crosstalk Between X-ray Irradiated Caco-2 Cells and PBMC

Published on: January 30, 2018

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

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

  • Examination of cardiovascular risks associated with COX-2 inhibitors (coxibs).

    • Main Results:

    • NSAID efficacy is linked to COX-2 inhibition.
    • COX-1 inhibition causes side effects like gastrointestinal bleeding and renal failure.
    • Selective COX-2 inhibitors (coxibs) have been associated with increased thrombotic cardiovascular events since 2004.

    Conclusions:

    • Selective COX-2 inhibition presents a therapeutic challenge due to cardiovascular risks.
    • Further research into COX enzyme biology is needed for safer anti-inflammatory strategies.
    • Understanding the role of COX in atherosclerosis is critical for patient management.