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

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

722
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
722
Transducer Mechanism: G Protein–Coupled Receptors01:30

Transducer Mechanism: G Protein–Coupled Receptors

7.2K
G Protein–Coupled Receptors (GPCRs) are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to various stimuli. GPCRs regulate critical physiological pathways and are excellent drug targets for treating diseases such as diabetes, cancer, obesity, depression, or Alzheimer's. Nearly 35% of approved drugs implement their therapeutic effects by selectively interacting with specific GPCRs.
GPCRs are also called heptahelical,...
7.2K
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

1.5K
Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
1.5K
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

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

1.5K
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...
1.5K
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

65
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
65
Drug-Receptor Interactions01:29

Drug-Receptor Interactions

8.2K
Drug-receptor interaction describes the binding of receptors by drugs, but not all drug-receptor interactions result in activation and tissue response. For instance, the binding of agonists activates the receptor to generate a cellular reaction, while antagonists bind to receptors without causing their activation.
Several parameters, such as the drug's affinity for its receptor and its efficacy, which is its ability to activate the receptor, determine the drug's effect on the tissue....
8.2K

You might also read

Related Articles

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

Sort by
Same author

Myofibroma of the distal biceps brachii tendon: imaging findings of a rare entity.

Journal of ultrasound·2026
Same author

Viscoelastic Tests in Cirrhotic Patients Undergoing Invasive Procedures: A Systematic Review and Meta-Analysis of RCTs.

Liver international : official journal of the International Association for the Study of the Liver·2026
Same author

Real-World Effectiveness of Baricitinib in Rheumatoid Arthritis: Significant Reduction of Disease Activity Independent of Age in a Multicentre Retrospective Cohort Study.

Mediterranean journal of rheumatology·2026
Same author

Management of Antiplatelet and Anticoagulant Therapy in the Context of Ultrasound-Guided Invasive Procedures.

Thrombosis and haemostasis·2026
Same author

Six months predictors of DAPSA Remission With Guselkumab in Psoriatic Arthritis in a Multicenter Real-World Study.

Scientific reports·2026
Same author

OUtcome and Clinical Characteristics of Primary Headache in Patients with Sarcoidosis: The OUCH! Study.

Life (Basel, Switzerland)·2026

Related Experiment Video

Updated: Mar 22, 2026

Author Spotlight: Enhanced Method for Evaluating Analgesic Effects — Dual Hind Paw Carrageenan Injection in Mice
06:54

Author Spotlight: Enhanced Method for Evaluating Analgesic Effects — Dual Hind Paw Carrageenan Injection in Mice

Published on: November 15, 2024

2.9K

The Coxib case: Are EP receptors really guilty?

Francesca Santilli1, Andrea Boccatonda1, Giovanni Davì1

  • 1Department of Internal Medicine, "G. d'Annunzio" University, Chieti, Italy.

Atherosclerosis
|April 23, 2016
PubMed
Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX) enzymes. Selective COX-2 inhibitors, like Coxibs, increase cardiovascular risk and cause adverse effects by altering prostaglandin synthesis and nitric oxide pathways.

Keywords:
CoxibEP receptorNSAIDsPlateletProstaglandin

More Related Videos

Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs
12:44

Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs

Published on: January 27, 2023

4.6K
Analysis of Raw and Processed Cyperi Rhizoma Samples Using Liquid Chromatography-Tandem Mass Spectrometry in Rats with Primary Dysmenorrhea
07:36

Analysis of Raw and Processed Cyperi Rhizoma Samples Using Liquid Chromatography-Tandem Mass Spectrometry in Rats with Primary Dysmenorrhea

Published on: December 23, 2022

2.0K

Related Experiment Videos

Last Updated: Mar 22, 2026

Author Spotlight: Enhanced Method for Evaluating Analgesic Effects — Dual Hind Paw Carrageenan Injection in Mice
06:54

Author Spotlight: Enhanced Method for Evaluating Analgesic Effects — Dual Hind Paw Carrageenan Injection in Mice

Published on: November 15, 2024

2.9K
Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs
12:44

Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs

Published on: January 27, 2023

4.6K
Analysis of Raw and Processed Cyperi Rhizoma Samples Using Liquid Chromatography-Tandem Mass Spectrometry in Rats with Primary Dysmenorrhea
07:36

Analysis of Raw and Processed Cyperi Rhizoma Samples Using Liquid Chromatography-Tandem Mass Spectrometry in Rats with Primary Dysmenorrhea

Published on: December 23, 2022

2.0K

Area of Science:

  • Pharmacology
  • Cardiovascular Medicine
  • Nephrology

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) exert effects by inhibiting cyclooxygenase (COX) enzymes, which are responsible for prostaglandin synthesis from arachidonic acid.
  • COX has two isoforms: COX-1 and COX-2. Selective inhibition of COX-2 is linked to increased cardiovascular (CV) risk.

Purpose of the Study:

  • To explore the mechanisms underlying the adverse effects of NSAIDs, particularly COX-2 selective inhibitors (Coxibs).
  • To investigate the role of prostaglandin synthesis, nitric oxide (NO) bioavailability, and related pathways in NSAID-induced vascular side effects.

Main Methods:

  • Review of existing literature on NSAID mechanisms, COX isoforms, and associated clinical outcomes.
  • Analysis of how drug concentration influences COX isoform selectivity and tissue-specific effects.
  • Examination of the interplay between prostaglandin pathways, NO/NOS system, and the renin-angiotensin-aldosterone system in NSAID toxicity.

Main Results:

  • Coxibs promote a prothrombotic state, increasing risks of myocardial infarction and stroke, and can counteract antihypertensive medications.
  • NSAIDs, including Coxibs, impair kidney function by disrupting glomerular filtration and salt/water balance.
  • Observed side effects of Coxibs include acute hepatitis, hyperkalemia, and atrial fibrillation, linked to prostaglandin pathway dysregulation.
  • The interaction between NSAIDs and COX enzymes is concentration-dependent, affecting different tissues uniquely.
  • Activation of E-type prostanoid (EP) receptors and alterations in NO bioavailability, influenced by NOS inhibitors like ADMA and l-NMMA, contribute to vascular side effects.

Conclusions:

  • NSAID-induced prostaglandin modifications, synergizing with changes in NO bioavailability and hormonal pathways, critically regulate vascular side effects.
  • Understanding these complex interactions is crucial for predicting and mitigating NSAID-related adverse events, especially cardiovascular and renal complications.