Evidence map›Paper›PMID 11930903›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2002

Gastric toxicity of racemic ketoprofen and its enantiomers in rat: oxygen radical generation and COX-expression.

C Alarcón de la Lastra, A Nieto, M J Martín, F Cabré, J M Herrerías, V Motilva

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.9field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 29 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

C Alarcón de la LastraDepartamento de Farmacología, Facultad de Farmacia, Sevilla, Spain. alarcon@fafar.us.es
A Nieto
M J Martín
F Cabré
J M Herrerías
V Motilva
Universidad de Sevilla · ESHospital de Sant Joan Despí Moisès Broggi · ESHospital Universitario Virgen Macarena · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

OBJECTIVE AND

designThe gastric toxicity of racemic-ketoprofen and its enantiomers (S(+)- and R(-)-ketoprofen), oxygen free radical generation and neutrophil infiltration in response to damage were evaluated in rats. Changes in prostaglandin synthesis, cyclooxygenase expression and glutathione metabolism were also studied. MATERIALS AND

methodsStudies were performed in Wistar rats. Drugs were given by oral administration: racemic-ketoprofen (100, 50 and 25 mg/kg body weight); S(+) and R(-)-ketoprofen (50, 25 and 12.5 mg/kg body weight). Determinations were made of gastric mucosal injury, lipid peroxidation, xanthine oxidase, myeloperoxidase and superoxide dismutase activities, glutathione levels, glutathione peroxidase and glutathione reductase activities, gastric prostaglandin synthesis (PGE2 levels) and COX-expression.

resultsRacemic-ketoprofen dose-dependently exhibited the highest toxicity. In contrast, S(+)-ketoprofen at half the dose of the racemic compound proved to be less ulcerogenic. R(-)-ketoprofen was also less ulcerogenic, but when administered as the racemate exacerbated gastric ulceration caused by S(+)-ketoprofen. Drug administration produced significant increases in lipid peroxidation levels and xanthine-oxidase and a decrease in superoxide dismutase activity. Nevertheless the racemate induced the highest disturbances in oxidative metabolism. No changes in myeloperoxidase values and glutathione metabolism were found. Cyclooxygenase-1 immunoreactivity was observed and did not differ from that in control rats. Cyclooxygenase-2 could also be expressed after treatments.

conclusionsR(-)-ketoprofen and S(+)-ketoprofen have a comparable gastric toxicity and they both have a better gastric toxicity profile as compared to the racemate. In addition to inhibition of prostaglandin synthesis, damage resulted in an increase of cyclooxygenase-2 protein expression. Oxygen radicals, including superoxide anions, could also be implicated.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCyclooxygenase 1Cyclooxygenase 2DinoprostoneFemaleGastric MucosaGlutathioneIsoenzymesKetoprofenMaleMembrane ProteinsNeutrophilsProstaglandin-Endoperoxide SynthasesRatsRats, WistarAnti-Inflammatory Agents, Non-SteroidalCyclooxygenase 1Cyclooxygenase 2DinoprostoneGlutathioneIsoenzymesKetoprofenMembrane ProteinsProstaglandin-Endoperoxide SynthasesPtgs1 protein, ratReactive Oxygen SpeciesThiobarbituric Acid Reactive Substances

Identifiers

PMID11930903
OpenAlexW1994139521

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.