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  • 1
    Electronic Resource
    Electronic Resource
    Effects of meloxicam on oxygen radical generation in rat gastric mucosa (2000)
    Springer
    Inflammation research 49 (2000), S. 361-366 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Non-steroidal anti-inflammatory drugs (NSAIDs) – Meloxicam – COX-2 inhibitors – Gastric injury – Oxygen radical
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Aim and Design: In addition to a deficiency of endogenous prostaglandins due to inhibition of cyclo-oxygenase and a host of prostaglandin-mediated effects on mucosal protection, it has recently been proposed that neutrophil- and oxygen radical - dependent microvascular injuries may be important prime events that lead to mucosal injury induced by non-steroidal anti-inflammatory drugs. Therefore, we evaluated the role of oxygen free radicals in the pathogenesis of acute gastric ulceration induced by meloxicam, a preferential COX-2 inhibitor.¶Material: Studies were performed in Wistar rats.¶Treatment: Meloxicam was given by oral administration (3.75-30 mg/kg body weight).¶Methods: Determinations were made of gastric mucosal injury, xanthine-oxidase, myeloperoxidase and superoxide dismutase activities, as well as the effect of meloxicam on gastric prostaglandin synthesis (PGE2 levels) and glutathione homeostasis.¶Results: Oral administration of meloxicam dose-dependently (3.75-30 mg/kg) caused acute gastric haemorrhage erosions. The total area of gastric lesions increased with time until 24 hours after dosing. Xanthine-oxidase activity increased significantly after administration of the drug. Myeloperoxidase activity, as an index of neutrophil infiltration, as well as glutathione peroxidase, an important enzyme that scavenges lipid peroxides, were unaffected by meloxicam administration. In addition, superoxide dismutase activity, PGE2 and glutathione levels were significantly reduced.¶Conclusion: These results support the hypothesis that in addition to suppresion of prostaglandin synthesis, oxygen free radicals, probably derived via the action of xanthine oxidase, the decrease in superoxide dismutase activity, and the depletion of mucosal glutathione contribute to the pathogenesis of meloxicam-induced ulceration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00000217
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  • 2
    Electronic Resource
    Electronic Resource
    Intestinal toxicity of ketoprofen-trometamol vs its enantiomers in rat. Role of oxidative stress (2000)
    Springer
    Inflammation research 49 (2000), S. 627-632 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Ketoprofen – Dexketoprofen – Intestinal effects – Stereoselectivity – NSAIDs – Refed rats – Oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: Objective: Gastrointestinal damage and bleeding are the major side effects of non-steroidal anti-inflammatory drugs (NSAID), however the mechanisms of this ulcerogenic action are not fully understood. It has recently been proposed that neutrophil-and oxygen radical-dependent microvascular injuries may be important prime events that lead to mucosal injury. In addition, other factors like bile flow, intact bacterial flora or feeding conditions may contribute to the formation of lesions. Ketoprofen is a NSAID that exists as a pair of R(-) and S(+) enantiomers; like other 2-arylpropionic acids, its anti-inflammatory effects resides almost exclusively in the S(+) isomer. The present study was undertaken to explore the role of oxidative stress in the pathogenesis of intestinal injury induced by oral administration of racemic ketoprofen and its enantiomers given as their water soluble tromethamine salts.¶Material and methods: Evaluation of intestinal damage and activities of oxidative stress related enzymes such as myeloperoxidase (MPO), xanthine-oxidase (XO) and superoxide dismutase (SOD) were studied in an experimental animal model using refed rats.¶Results: After the oral treatment followed by a refeeding period of 24 h, ketoprofen (100, 50, 25 mg/Kg b.w.) dose-dependently caused longitudinal ulcers on the mesenteric side of the middle and lower intestine lumen. The intestinal toxicity caused by S(+)-ketoprofen was significantly lower than the effect observed after racemate and R(-) enantiomer treatments (P〈0.001), though the bioinversion of R(-)-ketoprofen to S(+)-enantiomer that occurs in the rat has to be considered. XO activity was unaffected by the studied drugs. Enhanced enteropathy by the racemate and its R(-)-enantiomer was correlated with a significant increase of MPO activity as an index of neutrophil infiltration, and a decrease in SOD activity (p〈0.05 Vs control). S(+)-ketoprofen did not significantly change these parameters.¶Conclusions: These results suggest that reactive oxygen metabolites can contribute significantly to the development of intestinal lesions, and that R(-)-ketoprofen present in racemic preparations can enhance the toxic intestinal effects of S(+)-enantiomer via modification of neutrophil migration and oxidative stress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050640
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  • 3
    Electronic Resource
    Electronic Resource
    Role of endogenous sulphydryls and neutrophil infiltration in the pathogenesis of gastric mucosal injury induced by piroxicam in rats (1996)
    Springer
    Inflammation research 45 (1996), S. 83-88 
    Details
    ISSN: 1420-908X
    Keywords: NSAIDs ; Piroxicam ; Gastric ulcer ; Neutrophils ; Sulphydryl compounds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the present report we studied the formation of severe gastric erosions produced in fasted rats by intragastric administration of piroxicam (PRX), an enolic acid-derived NSAID. The time course of gastric damage and the possible role of mucus secretion, endogenous sulphydryl compounds, changes of gastric vascular permeability and neutrophil infiltration in the development of PRX-induced gastric lesions were also investigated. PRX dose-dependently (1.25–20 mg/kg) caused acute gastric haemorrhagic erosion in the rat. The lesions increased with time until 9 hr after dosing. Mucus secretion did not change significantly with respect to the control group with 5, 10 and 20 mg/kg of PRX at different times (3 and 6 hours) of treatment. There was also no increase in the concentration of its components. In addition, oral pretreatment of the animals with PRX did not significantly change the amount of dye trapped in the stomach. In contrast, non-protein SH fraction was decreased after administration of PRX and MPO activity as an index of neutrophil infiltration was significantly increased. These results suggest that independently of the PRX dose, depletion of endogenous non-protein SH and neutrophil infiltration could play an important part in the pathogenesis of gastric mucosal injury induced by PRX.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02265120
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of cinitapride on gastric ulceration and secretion in rats (1998)
    Springer
    Inflammation research 47 (1998), S. 131-136 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Cinitapride — 5-hydroxytryptamine — Gastric ulceration — Neutrophils — Oxygen free radicals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective and Design: The aim of the present study was to examine the effects of cinitapride, a novel prokinetic benzamide-stimulating gastrointestinal motility agent, on gastric secretion and ulceration in rats and elucidate some possible vascular and anti-oxidant mechanisms of such protection.¶Material: Male Wistar rats.¶Treatment: Cinitapride (CNT, Lab. Almirall, S.A.) (0.25, 0.5, and 1 mg/kg) and 5-hydroxytryptamine (5-HT, Sigma Chemical Co., St. Louis, MO, USA) (10 mg/kg), administered intraperitoneally (i.p.).¶Methods: Gastric ulceration was induced by instillation of 1 mL/100 g animal of 50% (v/v) ethanol in distilled water and by pylorus-ligated rat model. Gastric microvascular changes, and the activity of myeloperoxidase (as a marker of neutrophil infiltration) and glutathione peroxidase (an important enzyme in scavenging of lipid peroxides) were determined. The results were compared with those of 5-HT. The data were evaluated using Student’s t-test for paired data and the non-parametric Mann-Whitney U-test.¶Results: In 4 h pyloric-ligated animals, i.p. CNT did not significantly reduce the incidence of gastric mucosal damage, and no significant differences were found in the values of total volume and acidity. However, CNT caused a marked and dose-dependent reduction of haemorrhagic lesions induced by 50% v/v ethanol. These protective effects were specifically related to a reduction of neutrophil infiltration. CNT at the dose of 1 mg/kg raised the decreased glutathione peroxidase activity to the control level. In contrast, pretreatment with 5-HT worsened the ethanol-induced erosions, but did not significantly induce any gastric microvascular changes. However, the myeloperoxidase activity rose markedly and the glutathione peroxidase levels decreased significantly in the mucosa injured by 50% v/v ethanol.¶Conclusions: This study demonstrates a new gastroprotective feature of CNT that could be partly explained not only through reduction of neutrophil toxicity but also by an increased synthesis of free-radical scavenging enzymes such as glutathione peroxidase. Furthermore, it is likely that serotonergic-dependent mechanisms are also involved via 5-HT2-receptor blockade and 5-HT1 receptor activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050301
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