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 Experiment Videos

NSAID-induced gastroenteropathy: a biochemical dissection.

P J Russo1, N W Seidler

  • 1University of Health Sciences, College of Osteopathic Medicine-Kansas City, Mo.

Hospital Practice (Office Ed.)
|December 15, 1992
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Endogenous plastic composite material in the Alzheimer's brain.

Medical hypotheses·2006
Same author

Glycation of aspartate aminotransferase and conformational flexibility.

Biochemical and biophysical research communications·2000
Same author

Non-enzymatic glycosylation (or glycation) and inhibition of the pig heart cytosolic aspartate aminotransferase by glyceraldehyde 3-phosphate.

Journal of enzyme inhibition·2000
Same author

Carnosine prevents the glycation-induced changes in electrophoretic mobility of aspartate aminotransferase.

Journal of biochemical and molecular toxicology·2000
Same author

Carnosine prevents glyceraldehyde 3-phosphate-mediated inhibition of aspartate aminotransferase.

Archives of toxicology·1999
Same author

Inhibition of the cardiac sarcoplasmic reticulum Ca2+-ATPase by glucose 6-phosphate is Ca2+ dependent.

Life sciences·1998

Non-steroidal anti-inflammatory drugs (NSAIDs) may cause gastrointestinal lesions primarily through microvascular damage, challenging the traditional view of mucosal damage being the initial step. This research explores the underlying mechanisms of NSAID-induced gastrointestinal injury.

Area of Science:

  • Gastroenterology
  • Pharmacology
  • Pathology

Background:

  • Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly associated with gastrointestinal (GI) lesions.
  • The prevailing hypothesis attributes NSAID-induced GI damage to direct mucosal injury.
  • An alternative perspective suggests NSAID-induced damage to the GI microvasculature as the primary event.

Purpose of the Study:

  • To investigate the role of NSAID-induced microvascular damage in the pathogenesis of GI lesions.
  • To challenge the established understanding of NSAID-induced mucosal injury.

Main Methods:

  • This study likely involves preclinical models or in vitro assays to assess microvascular integrity and mucosal changes following NSAID administration.
  • Histopathological examination and biochemical analyses may be employed to differentiate between mucosal and microvascular damage.

Related Experiment Videos

Main Results:

  • Results are expected to provide evidence supporting or refuting the hypothesis that microvascular damage precedes or is the primary cause of NSAID-related GI lesions.
  • Comparative analysis of mucosal integrity and microvascular changes under NSAID influence.

Conclusions:

  • The findings will elucidate the primary mechanism of NSAID-induced GI injury, potentially shifting the therapeutic and preventive strategies.
  • Understanding the precise pathogenic pathway is crucial for mitigating the adverse effects of NSAIDs.