ArticleInflammation1992
Pharmacological investigation of the role of leukotrienes in the pathogenesis of experimental NSAID gastropathy.
Article in Inflammation, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 78 citations in OpenAlex.
- Gastroprotective effect of zafirlukast against indomethacin induced gastric ulcer in rats via PGE2 and anti-inflammatory pathways.Iranian journal of basic medical sciences · 2023Article
- Pain killers: the interplay between nonsteroidal anti-inflammatory drugs and Clostridioides difficile infection.Current opinion in microbiology · 2022Review
- Eicosanoids in the gastrointestinal tract.British journal of pharmacology · 2019Review
- Efficacy of a Peruvian Botanical Remedy (Sabell A4+) for Treating Liver Disease and Protecting Gastric Mucosal Integrity.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Potassium Channelopathies and Gastrointestinal Ulceration.Gut and liver · 2016Review
- Rationally designed multitarget agents against inflammation and pain.Current medicinal chemistry · 2013Review
- Current perspectives in NSAID-induced gastropathy.Mediators of inflammation · 2013Review
- Lack of effects of acemetacin on signalling pathways for leukocyte adherence may explain its gastrointestinal safety.British journal of pharmacology · 2008Article
- Mechanisms underlying the anti-inflammatory activity and gastric safety of acemetacin.British journal of pharmacology · 2007Article
- Increased susceptibility of ethanol-treated gastric mucosa to naproxen and its inhibition by DA-9601, an Artemisia asiatica extract.World journal of gastroenterology · 2005Article
- Current approaches to prevent NSAID-induced gastropathy--COX selectivity and beyond.British journal of clinical pharmacology · 2004Review
- Inhibition of the arachidonic acid cascade by norathyriol via blockade of cyclooxygenase and lipoxygenase activity in neutrophils.Naunyn-Schmiedeberg's archives of pharmacology · 2004Article
- Gastrosparing effect of new antiinflammatory drug amtolmetin guacyl in the rat: involvement of nitric oxide.Digestive diseases and sciences · 1999Article
- Article
- Cyclo-oxygenase isoenzymes. How recent findings affect thinking about nonsteroidal anti-inflammatory drugs.Drugs · 1997Review
- Chronic effects of misoprostol in combination with the NSAID, diclofenac, on gastrointestinal tract of pigs. Relation to diarrheagenic activity, leukocyte infiltration, and mucosal leukotrienes.Digestive diseases and sciences · 1995Article
- Leukotrienes do not contribute to the pathogenesis of indomethacin-induced ulceration of the gastric antrum in the re-fed rat.Agents and actions · 1994Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of leukotrienes in the pathogenesis of acute gastric ulceration induced by nonsteroidal antiinflammatory drugs was investigated using a rat model. One part of the study involved oral pretreatment with a leukotriene synthesis inhibitor 1 h prior to administration of indomethacin (20 mg/kg per os). Three hours after indomethacin, the extent of macroscopically visible gastric damage was determined, and gastric LTB4 synthesis was determined. The compounds tested were PF-5901, A-64077, nordihydroguaiaretic acid, and L-698,037. Each compound produced dose-related inhibition of gastric LTB4 synthesis and a parallel reduction in the severity of indomethacin-induced damage. The antioxidant properties of these compounds was assessed using an in vitro assay. There was no correlation between the antioxidant properties of the compounds and their ability to reduce the severity of indomethacin-induced gastric damage. In the second part of the study, the effects of intravenous, administration of LTD4 and LTB4 receptor antagonists on indomethacin-induced gastric epithelial damage (measured by permeability to [51Cr]EDTA) were assessed. The two LTD4 receptor antagonists (MK-571 and ICI-204,219) significantly reduced the permeability changes induced by indomethacin, while the two LTB4 antagonists (SC-41930 and LY-255,283) were without significant effect. Despite the reduction of gastric epithelial injury, blockade of LTD4 receptors did not markedly affect the extent of macroscopically visible injury. These data are consistent with the hypothesis that leukotrienes contribute to the epithelial injury and macroscopically visible damage induced by NSAIDs. However, it remains unclear to what extent leukotrienes are involved in the initiation of the injury, as opposed to its amplification.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.