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

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...
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...
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,...
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...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...

You might also read

Related Articles

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

Sort by
Same author

Enhancing safety and compliance in acute behavioural disturbance management: Pilot of proposed update to zuclopenthixol acetate guidelines in a regional PICU.

Australasian psychiatry : bulletin of Royal Australian and New Zealand College of Psychiatrists·2026
Same author

The correlation of cardiovascular magnetic resonance imaging findings with clinical diagnoses and its acute impact on management changes in a regional Australian hospital.

Medicine·2026
Same author

ACTIVATE: physical activity assessment, prescription and promotion in clinical practice by healthcare professionals - a consensus study initiated by the International Federation of Sports Physical Therapy.

British journal of sports medicine·2026
Same author

RNAseq Analysis of the Cerebellum Reveals Significant Gene Dysregulation That May Explain Chronic Disease Progression in Mild Traumatic Brain Injury.

Journal of neuroscience research·2026
Same author

Enhancing mental health care: Referrer satisfaction with consultation liaison psychiatry service in a regional Australian hospital.

Australasian psychiatry : bulletin of Royal Australian and New Zealand College of Psychiatrists·2025
Same author

Challenges of Dementia Care in a Regional Australian Hospital: Exploring Interventions to Minimise Length of Stay for Dementia Patients.

The Australian journal of rural health·2024

Related Experiment Video

Updated: Jun 20, 2026

Acute Brain Trauma in Mice Followed By Longitudinal Two-photon Imaging
11:14

Acute Brain Trauma in Mice Followed By Longitudinal Two-photon Imaging

Published on: April 6, 2014

12.4K

Selective COX-2 Inhibitors as Neuroprotective Agents in Traumatic Brain Injury.

Matthew I Hiskens1, Anthony G Schneiders2, Andrew S Fenning2

  • 1Mackay Institute of Research and Innovation, Mackay Hospital and Health Service, Mackay, QLD 4740, Australia.

Biomedicines
|August 29, 2024
PubMed
Summary
This summary is machine-generated.

Cyclooxygenase-2 (COX-2) inhibitors show promise in treating traumatic brain injury (TBI) by reducing inflammation and cell death. Early studies suggest these COX-2 inhibitors may improve patient outcomes following TBI.

Keywords:
cyclooxygenaseinflammationneuroinflammationneuroprotectiontraumatic brain injury

More Related Videos

Controlled Cortical Impact Model for Traumatic Brain Injury
05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

28.5K
A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

1.8K

Related Experiment Videos

Last Updated: Jun 20, 2026

Acute Brain Trauma in Mice Followed By Longitudinal Two-photon Imaging
11:14

Acute Brain Trauma in Mice Followed By Longitudinal Two-photon Imaging

Published on: April 6, 2014

12.4K
Controlled Cortical Impact Model for Traumatic Brain Injury
05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

28.5K
A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

1.8K

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Traumatic brain injury (TBI) is a leading cause of death and disability.
  • Currently, no specific therapies exist for TBI.
  • Inflammation and cell death following TBI contribute to secondary injury.

Purpose of the Study:

  • To review the therapeutic effects of COX-2 inhibitors in TBI.
  • To explore the molecular pathways and mechanisms of action.
  • To assess the clinical evidence for COX-2 inhibitors in TBI patients.

Main Methods:

  • Review of animal models of TBI.
  • Analysis of studies on selective COX-2 inhibitors.
  • Examination of clinical trial data.

Main Results:

  • COX-2 inhibition reduces neuroinflammation and neuronal cell death in TBI models.
  • Selective COX-2 inhibitors demonstrate neuroprotective potential.
  • Early clinical trials indicate improved mortality and outcomes with celecoxib use.

Conclusions:

  • COX-2 inhibitors represent a potential therapeutic strategy for TBI.
  • Further research is warranted to fully elucidate their efficacy and safety in patients.