Role of tumor necrosis factor α release and leukocyte margination in indomethacin-induced gastric injury in rats

Santucci, Luca; Fiorucci, Stefano; Matteo, Francesco Maria Di; Morelli, Antonio

doi:10.1016/0016-5085(95)90065-9

Cited by 142 publications

(103 citation statements)

References 24 publications

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“…It is likely the latter occurred through increased expression of adhesion molecules on both PMN and endothelial cells, leading to tissue ischemia (Santucci et al 1995). Results here showed that fluoxetine pre-treatment significantly prevented increases in TNF levels in both models; this would support an antiinflammatory effect of fluoxetine noted in previous studies (Abdel-Salam et al 2003;Mozaffari et al 2011).…”

Section: Discussionsupporting

confidence: 84%

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats

Sokar

Elsayad

Ali

2016

Journal of Immunotoxicology

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Research in the treatment of gastric ulcer has involved the investigation of new alternatives, such as anti-depressant drugs. The present study was designed to investigate the gastroprotective effects of fluoxetine against indomethacin and alcohol induced gastric ulcers in rats and the potential mechanisms of that effect. Fluoxetine (20 mg/kg) was administered IP for 14 days. For comparative purposes, other rats were treated with ranitidine (30 mg/kg). Thereafter, after 24 h of fasting, INDO (100 mg/kg) or absolute alcohol (5 ml/kg) was administered to all rats (saline was administered to naïve controls) and rats in each group were sacrificed 5 h (for INDO rats) or 1 h (for alcohol rats) later. Macroscopic examination revealed that both fluoxetine and ranitidine decreased ulcer scores in variable ratios, which was supported by microscopic histopathological examination. Biochemical analysis of fluoxetine-or ranitidine-pre-treated host tissues demonstrated reductions in tumor necrosis factor (TNF)-and myeloperoxidase (MPO) levels and concomitant increases in gastric pH, nitric oxide (NO) and reduced glutathione (GSH) contents. Fluoxetine, more than ranitidine, also resulted in serotonin and histamine levels nearest to control values. Moreover, immuno-histochemical analysis showed that fluoxetine markedly enhanced expression of cyclooxygenases COX-1 and COX-2 in both models; in comparison, ranitidine did not affect COX-1 expression in either ulcer model but caused moderate increases in COX-2 expression in INDOinduced hosts and high expression in alcohol-induced hosts. The results here indicated fluoxetine exhibited better gastroprotective effects than ranitidine and this could be due to anti-secretory, anti-oxidant, anti-inflammatory and anti-histaminic effects of the drug, as well as a stabilization of gastric serotonin levels. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 84%

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats

Sokar

Elsayad

Ali

2016

Journal of Immunotoxicology

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“…20 Aspirin induces the reactive oxygen metabolites in animal models, which may contribute to mucosal injury. Oxygen-derived free radicals play a key role in the mechanism of aspirin-induced acute gastric mucosal lesions.…”

Section: Discussionmentioning

confidence: 99%

The effect of aspirin nanoemulsion on TNFα and iNOS in gastric tissue in comparison with conventional aspirin

Mahmoud¹,

Hashem²,

Elkelawy³

2015

IJN

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Background No dose of aspirin is free of bleeding risk. Even at a dose as low as 75 mg/day, the risk of upper gastrointestinal bleeding is twice as high as among nonusers. Nanoemulsions (NEs) are emulsion systems with droplet size in nanometer scale in which oil or water droplets are finely dispersed in the opposite phase with the help of a suitable surfactant to stabilize the system. Objectives The objective of this study was to determine the effect of aspirin NE in comparison to conventional aspirin. Materials and methods A total of 24 male rats were used in the study and arbitrarily assigned to four groups. Group 1 was the control group, and was given saline. Group 2 was given blank NE 1.5 mL/kg orally. Group 3 was given aspirin 30 mg/kg body weight orally. Group 4 was given aspirin NE 30 mg/kg body weight orally. Rats were killed, and gastric tissue was quickly excised after dissection of the animals. The tissues were divided into three pieces. The first one was kept in formalin 10% for pathological investigation. The second piece was kept in liquid nitrogen for molecular investigation. The third piece was homogenized in ten volumes of ice-cold phosphate-buffered saline (pH 7) using a Teflon homogenizer until a uniform suspension was obtained. The homogenate was centrifuged at 4,000 rpm for 30 minutes at 4°C to separate the supernatant from cellular debris. The supernatant was then used for the estimation of biochemical assays. Results The present study shows that aspirin has a toxic effect on the stomach as a result of inducing marked oxidative damage and the release of reactive oxygen species. This was shown by the significant increase in TNFα, iNOS, prostaglandin E 2 , and malondialdehyde levels, and also a significant decrease in glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase. In the aspirin-treated group compared to the control group, the NE had a protective effect on the stomach and caused less injury than aspirin, indicated by significant decreases in TNFα, iNOS, prostaglandin E 2 , and malondialdehyde levels, and also significant increases in glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase. The biochemical results were confirmed by histopathological studies. Conclusion Aspirin nanoemulsion has less toxic effect on the gastric mucosa compared to ordinary aspirin. This can be indicated by the increase of the antioxidant activity and the decrease of the inflammatory mediators in the gastric tissue.

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“…12 This is in contrast to the indomethacininduced gastropathy which is associated with elevations in TNF concentration, thus the mechanism of action of pentoxifylline may be different in indomethacin-induced injury compared to the TNBS-induced injury model. 13 A systematic study of cytokine levels in animals treated with TNBS would, at best, show an association between colonic damage and cytokine levels but would not indicate a causative nature. A more appropriate study would involve the blocking of speci®c cytokines and growth factors with antibodies.…”

Section: Discussionmentioning

confidence: 99%

Effect of acute pentoxifylline treatment in an experimental model of colitis

Peterson

Davey

1997

Aliment Pharmacol Ther

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INTRODUCTIONIn the present study the animal model of in¯ammatory bowel disease is caused by the agent trinitrobenzene sulphonic acid (TNBS). This was ®rst used in 1989 by Morris et al., and is based on the hypothesis of Ward Shorter et al. which presumes that an increase in mucosal permeability in Crohn's disease results in entry into the lamina propria of a luminal antigen that is not adequately cleared by the mucosal immune system. 1±3 Instillation of a solution containing ethanol and TNBS into the distal colon of the rat elicits an immune response. The ethanol acts as a barrier breaker while TNBS acts as the hapten with resulting development of severe transmural granulomatous in¯ammation similar to that seen in in¯ammatory bowel disease. In this animal model we assess the effects of pentoxifylline, a methylxanthine which has been reported to reduce in¯ammation in other animal models and to block ®brosis in animal models of hepatic ®brosis. 4,5 Because of the association of in¯ammatory bowel disease with stricture formation, and the increased collagen deposition in SUMMARY Background: The effect of acute pentoxifylline treatment in an experimental model of colitis was assessed using the trinitrobenzene sulphonic acid (TNBS)-induced rat model of colitis. Methods: Animals were treated with intracolonic injection (250 lL) of TNBS (50 mg in 50% ethanol) to induce in¯ammation and ulcers. Animals received pentoxi®lline (100 mg/kg intracolonically) or saline 24 and 48 h following TNBS treatment. Five days following TNBS treatment, colons were dissected and scored according to the morphology damage score. The colons were then rolled longitudinally, ®xed in formalin and embedded in paraf®n. The collagen content of colonic sections was determined by a Sirius red±Fast green technique. Results: Animals treated with TNBS alone had signi®cantly higher gross morphology damage scores

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Role of tumor necrosis factor α release and leukocyte margination in indomethacin-induced gastric injury in rats

Cited by 142 publications

References 24 publications

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats

The effect of aspirin nanoemulsion on TNFα and iNOS in gastric tissue in comparison with conventional aspirin

Effect of acute pentoxifylline treatment in an experimental model of colitis

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Role of tumor necrosis factor α release and leukocyte margination in indomethacin-induced gastric injury in rats

Cited by 142 publications

References 24 publications

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats

The effect of aspirin nanoemulsion on TNF&alpha; and iNOS in gastric tissue in comparison with conventional aspirin

Effect of acute pentoxifylline treatment in an experimental model of colitis

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The effect of aspirin nanoemulsion on TNFα and iNOS in gastric tissue in comparison with conventional aspirin