NSAID-induced gastric damage in rats: requirement for inhibition of both cyclooxygenase 1 and 2.
By J. Wallace, W. McKnight, B. Reuter, N. Vergnolle. Gastroenterology, 2000
773 citations recorded by the source corpus.
Subfields: Pharmacology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/de875f300c9dfaaef0990a54547e61bfc0244f6b
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Maria Grazia Perrone
- A. Scilimati
- L. Simone
- Paola Vitale
- D. Simmons
- R. Botting
- Daniel Caminada
- A. Weston
Citations in the corpus
- Selective COX-1 inhibition: A therapeutic target to be reconsidered. (2010, background): “reported that gastric ulcers are not formed by COX-1 selective inhibition [130].”
- Ecotoxicology of human pharmaceuticals. (2006, background): “Gastric damages are thought to be caused by inhibition of both COX isoforms (Wallace, 1997; Wallace et al., 2000).”
- Cyclooxygenase Isozymes: The Biology of Prostaglandin Synthesis and Inhibition (2004, background): “Thus, it appears that inhibition of the activity of both COX-1 and COX-2 is required to produce gastric damage (Wallace et al., 2000).”
- Peptic ulcer disease. (2018, neutral): “Although not seems that the exclusive use of corticosteroids substantially increase the risk of ulcer bleeding, the combined use of these drugs together with NSAIDs, may increase by tenfold the risk of this complication [19,20].”