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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
Two synthetic agonists of THC,...
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...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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

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...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

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Related Experiment Video

Updated: Jun 2, 2026

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

Cannabinoid system and cyclooxygenases inhibitors.

H Păunescu1, O A Coman, L Coman

  • 1Department of Pharmacology and Pharmacotheraphy, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania. phpaunescu@yahoo.com

Journal of Medicine and Life
|April 21, 2011
PubMed
Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) can interact with the cannabinoid system through various mechanisms. This review summarizes NSAID-cannabinoid interactions, highlighting acetaminophen

Keywords:
NSAIDsanalgesiacannabinoidscyclooxygenase

Related Experiment Videos

Last Updated: Jun 2, 2026

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

Area of Science:

  • Pharmacology
  • Neuroscience
  • Biochemistry

Background:

  • The endocannabinoid system comprises receptors, endogenous ligands, and metabolic enzymes.
  • It interacts with other lipid mediator systems, such as prostaglandins and leukotrienes.
  • The precise effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on the cannabinoid system remain unclear.

Purpose of the Study:

  • To systematically review and summarize existing data on interactions between NSAIDs and the cannabinoid system.
  • To elucidate potential additive, antagonistic, or synergistic effects of combined NSAID-cannabinoid administration.

Main Methods:

  • Conducted a bibliographic research across Medline, Scirus, and Embase databases.
  • Utilized keywords including 'cannabinoid,' 'nonsteroidal anti-inflammatory drugs,' specific NSAID names (aspirin, ibuprofen, etc.), and related terms like 'analgesia'.

Main Results:

  • Acetaminophen (paracetamol) has been the most studied NSAID concerning its interference with the cannabinoid system, yielding inconsistent findings.
  • Certain NSAIDs inhibit fatty acid amide hydrolase (FAAH) or endocannabinoid transporters.
  • NSAIDs inhibiting cyclooxygenase-2 (COX-2) may influence the cannabinoid system due to potential COX-2 involvement in endocannabinoid degradation.

Conclusions:

  • NSAIDs exhibit diverse interactions with the cannabinoid system, including enzyme inhibition and transporter interference.
  • Variability in experimental outcomes may stem from pharmacokinetic factors like dosage and administration route.
  • Further research is needed to clarify the complex interplay between NSAIDs and the endocannabinoid system for therapeutic applications.