Mechanisms of gastroprotection by lansoprazole pretreatment against experimentally induced injury in rats: role of mucosal oxidative damage and sulfhydryl compounds

Natale, Gianfranco; Lazzeri, Gloria; Lubrano, Valter; Colucci, Rocchina; Vassalle, Cristina; Fornai, Matteo; Blandizzi, Corrado; Tacca, M. Del

doi:10.1016/j.taap.2003.10.006

Cited by 59 publications

(56 citation statements)

References 41 publications

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“…Moreover, rats treated with the combination of ranitidine and diclofenac showed decreased production of gastric acid and also decreased incidence of gastric ulcers. This may be attributed to the ranitidine's antioxidative potential as has been reported in previous studies (7,20,23) . Histologically too, ranitidine was observed to reduce gastric and liver damage which may be due to inhibition of neutrophil activation as observed in earlier studies (21,22) .…”

Section: • Change In Phsupporting

confidence: 71%

“…Previous studies have reported that NSAIDs may also induce gastric damage by acid-independent mechanisms such as by increasing oxidative stress parameters viz. increase in mucosal myeloperoxidase levels, together with increase in mucosal malondialdehyde and reduced glutathione concentration (7,20,23) . Malondialdehyde is an end product of the peroxidation of polyunsaturated fatty acids and related esters within cell membranes, such that the measurement of this compound represents a suitable index of oxidative tissue damage (15) .…”

Section: • Change In Phmentioning

confidence: 99%

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ADMINISTRATION OF H2 BLOCKERS IN NSAID INDUCED GASTROPATHY IN RATS: effect on histopathological changes in gastric, hepatic and renal tissues

Manocha

Lal

Venkataraman

2016

Arq. Gastroenterol.

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-Background -Nonsteroidal anti-inflammatory drugs induces gastric mucosal lesions because of its acidic properties.Ranitidine, an H 2 receptor antagonist, has proved beneficial in patients with gastric ulcers. Objective -The present study was performed to assess the effect of administering ranitidine in Nonsteroidal anti-inflammatory drugs (diclofenac, nimesulide) induced gastropathy, and their effect on the histopathology of stomach, kidney and liver. Methods -Diclofenac, nimesulide, and ranitidine were administered in doses of 2, 4, and 6 mg/kg, p.o. once daily for 14 days, and their effect on gastric volume, acidity, mean ulcer number, and gastric pH. In addition, histopathological examination was also performed on sections of stomach, kidney and liver.Results -Following the administration of diclofenac or nimesulide, all the gastric parameters were significantly altered as well as the histopathology of stomach, liver and kidney. In the control group, the renal sections showed normal glomeruli with no thickening of glomerular basement membrane, while in diclofenac alone, nimesulide alone, and ranitidine with nimesulide groups, the thickening of glomerular basement membrane was observed. These alterations were observed to be reversed in the ranitidine with diclofenac group. In the sections from the liver, the control group showed anastomosing plates and cords of cuboidal hepatocytes with round well stained nuclei and abundant cytoplasm. In the ranitidine with diclofenac, and ranitidine with nimesulide groups, mild dilatation of sinusoids is seen coupled with prominence of central vein. In the diclofenac alone and nimesulide alone groups, the proximal and distal convoluted tubules show mild focal tubular necrosis. In the gastric sections, the control group showed several folds forming villi, and the epithelial lining surface of the mucosa. In the ranitidine with diclofenac, and ranitidine with nimesulide groups, the duodenum showed scattered inflammatory cells composed predominantly of lymphocytes. In diclofenac alone and nimesulide alone group, the sections from the gastric areas showed partial necrosis and mild chronic inflammation respectively. Conclusion -The study, therefore, has provided therapeutic rationale towards simultaneous administration of H 2 receptor blocker ranitidine with diclofenac to be more beneficial as compared to ranitidine with nimesulide, to minimise the gastric intolerance of diclofenac in long term treatment of inflammatory conditions. HEADINGS -Diclofenac. Ranitidine. Histamine H 2 antagonist. Stomach diseases. Non-steroidal anti-inflammatory agents.

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Section: • Change In Phsupporting

confidence: 71%

Section: • Change In Phmentioning

confidence: 99%

ADMINISTRATION OF H2 BLOCKERS IN NSAID INDUCED GASTROPATHY IN RATS: effect on histopathological changes in gastric, hepatic and renal tissues

Manocha

Lal

Venkataraman

2016

Arq. Gastroenterol.

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“…Other reports have suggested that, in the presence of oxidative damage, PG could be converted into products of oxidation, such as 8-iso-PGF 2a (Natale et al 2004), that induce vasoconstriction and platelet aggregation that might enhance ulcerogenic actions of necrotizing agent and promote tissue oxidation (Sametz et al 2000). The effect of fluoxetine on gastric acid secretion and subsequently higher gastric pH compared to values in the untreated ulcer counterparts may be secondary to its effect on NO and COX enzymes.…”

Section: Discussionmentioning

confidence: 99%

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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“…PPI is also known to have protective effects on gastrointestinal mucosa without the inhibition of acid secretion [58][59][60]. Such protective effects have been reported to occur via anti-inflammatory effects such as the inhibition of IL-8 production and neutrophil infiltration and via cell injury repair through MAPK [61][62][63].…”

Section: Prevention and Treatment Of Small Intestinal Mucosal Injury mentioning

confidence: 99%

Present status and strategy of NSAIDs-induced small bowel injury

et al. 2009

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Non-steroidal anti-inflammatory drugs (NSAIDs) are well known to cause gastroduodenal mucosal lesions as an adverse effect. Recently, the serious problem of NSAID-induced small intestinal damage has become a topic of great interest to gastroenterologists, since capsule endoscopy and balloon enteroscopy are available for the detection of small intestinal lesions. Such lesions have been of great concern in clinical settings, and their treatment and prevention must be devised as soon as possible. The prevalence of NSAIDs-induced small intestinal injury is higher than had been expected. Recent studies show that more than 50% of patients taking NSAIDs have some mucosal damage in the small intestine. The gross appearance of NSAIDinduced enteropathy varies, appearing variously as diaphragm-like strictures, ulcers, erosions, and mucosal redness. To investigate NSAID-induced enteropathy, and to rule out other specific enteropathies, other useful methods (in addition to capsule endoscopy and balloon enteroscopy) include such modalities as radiological examination of the small intestine, the permeability test, scintigraphy or the fecal excretion test using 111 Indium-labeled white blood cells, and measurement of the fecal calprotectin concentration. Diaphragm-like strictures and bleeding from mucosal breaks may be treatable with interventional enteroscopy. Misoprostol, metronidazole, and sulfasalazine are frequently used to treat NSAID-induced enteropathy, but have undesirable effects in some cases. In the experimental model, we confirmed that several existing drugs for gastroduodenal ulcers prevented indomethacin-induced small intestinal injury. Such drugs may be useful for preventing the adverse effects of NSAIDs not only in the stomach but also in the small intestine. We hope to examine these drugs in future clinical studies.

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Mechanisms of gastroprotection by lansoprazole pretreatment against experimentally induced injury in rats: role of mucosal oxidative damage and sulfhydryl compounds

Cited by 59 publications

References 41 publications

ADMINISTRATION OF H2 BLOCKERS IN NSAID INDUCED GASTROPATHY IN RATS: effect on histopathological changes in gastric, hepatic and renal tissues

ADMINISTRATION OF H2 BLOCKERS IN NSAID INDUCED GASTROPATHY IN RATS: effect on histopathological changes in gastric, hepatic and renal tissues

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

Present status and strategy of NSAIDs-induced small bowel injury

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