Effects of omeprazole and gentamicin on the biochemical and histopathological alterations of the hypoxia/ reoxygenation induced intestinal injury in newborn rats

Bıçakçı, Ünal; Tander, Burak; Arıtürk, Ender; Aydin, Birsen Kilicoglu; Aydın, Oğuz; Rizalar, Rıza; Eren, Zafer; Bernay, Ferit

doi:10.1007/s00383-005-1538-y

Cited by 21 publications

(27 citation statements)

References 33 publications

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“…Omeprazole has antioxidant effects [13,14,31,32]. It also reduces polymorphonuclear leukocyte (PMNLs) chemotaxis and degranulation and the production of FOR.…”

Section: Discussionmentioning

confidence: 99%

“…H/R was done using airtight chamber. We modified our previously performed H/R model [13]. Rats were exposed to 100% CO 2 for 15 min followed by a reoxygenation for the next 15 min with 100% O 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Omeprazole is a H-K pump inhibitor used for gastric ulcer and gastroesophageal reflux. Omeprazole also has antioxidant properties [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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Protective effects of vitamin E and omeprazole on the hypoxia/reoxygenation induced intestinal injury in newborn rats

et al. 2008

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Evaluation of prophylactic effects of omeprazole and/or vitamin E on the formation of free oxygen radicals (FOR) and bowel histopathology in the newborn rat model of hypoxia/reoxygenation (H/R) that resembles human necrotizing enterocolitis (NEC). Eighty newborn rats were randomly divided into eight groups. H/R was done using airtight chamber. Rats were exposed to 100% CO2 for 15 min followed by a reoxygenation for the next 15 min with 100% O2. Group 1 (n = 10) was the control group. Group 2 (n = 10) rats received vitamin E. In Group 3 (n = 10) omeprazole was administrated. Group 4 (n = 10) rats received omeprazole and vitamin E. Group 5 (n = 10) rats were subjected to H/R two times for 2 days and one time for 3 days. Group 6 (n = 10) received vitamin E in addition to H/R for 5 days and in Group 7 (n = 10) omeprazole in addition to H/R for 5 days. In Group 8 (n = 10), vitamin E and omeprazole and H/R were applied for 5 days. Rats were killed at the end of the each process and bowel specimens were harvested for histopathological and biochemical investigations. We administrated vitamin E intramuscularly 300 unit/kg per day and omeprazole orally 20 mg/kg per day. Malondialdehyde (MDA), xanthine oxidase (XO), xanthine dehydogenase (XDH) and XO/(XO + XDH) were measured. Vitamin E and/or omeprazole treated rats had significantly less XO% levels than H/R only group (0.36, 0.38 and 0.57, respectively). Similarly, the MDA levels were significantly lower in vitamin E and/or omeprazole received rats than H/R only rats (88.8, 97.9 and 122.6, respectively). All rats treated with omeprazole and/or vitamin E had better biochemical and histopathological levels compared to H/R rats (p < 0.05). Histopathological results show that Group 5 (H/R only) had significantly more intestinal damage when compared with Group 6 (vitamin E + H/R), Group 7 (omeprazole + R/H) and Group 8 (vitamin E + omeprazole + H/R) (p < 0.001). Grade 2 and 3 intestinal damages were only in Group 5 and there were no statistical difference between in Groups 6, 7 and 8 (p > 0.001). Omeprazole and/or vitamin E may protect the biochemical and histopathological intestinal damage of H/R injury in rats. These drugs may be beneficial in the prophylaxis of NEC in humans as well.

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“…Omeprazole has antioxidant effects [13,14,31,32]. It also reduces polymorphonuclear leukocyte (PMNLs) chemotaxis and degranulation and the production of FOR.…”

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Protective effects of vitamin E and omeprazole on the hypoxia/reoxygenation induced intestinal injury in newborn rats

et al. 2008

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“…Recent reports have shown that P-ATPase inhibitors counteract inflammation by suppressing the expression of neutrophil and monocyte/MP adhesion molecules [8,9] and the production of ROS [10][11][12][13]. In addition, the clinical symptoms of Crohn's disease improved when patients were administered P-ATPase inhibitors [14,15].…”

Section: Introductionmentioning

confidence: 98%

Suppression of proinflammatory cytokine production in macrophages by lansoprazole

et al. 2006

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Macrophages (MPs) produce increased levels of proinflammatory cytokines in Crohn's disease; these cytokines are thought to play a central role in the occurrence of the disease. Biologics are currently available for anti-cytokine therapy, but treating intestinal inflammation through direct suppression of proinflammatory cytokine production could be more effective. P-ATPase inhibitors have been reported to be anti-inflammatory, and these inhibitors might suppress the production of MP proinflammatory cytokines. In this study, we examined the effect of two types of ATPase inhibitors on the expression patterns of typical proinflammatory cytokines. Peritoneal MPs from 6- to 8-week-old mice were cultured for 48 h in the presence of lansoprazole (P-ATPase inhibitor), bafilomycin A(1) (V-ATPase inhibitor), or the control solvent dimethylsulfoxide. The MPs were then examined for cytokine expression by quantitative real-time polymerase chain reaction (PCR), and culture supernatants were examined for cytokine production with a multiplex assay in a suspension array system. The possible existence of P-ATPase mRNA in MPs was explored using reverse-transcriptase PCR. P-ATPase mRNA was not detected in MP cells. However, all examined proinflammatory cytokines decreased significantly in their mRNA and protein expression in the lansoprazole-treated group. Conversely, bafilomycin A(1) increased the levels of these cytokines. Lansoprazole might be useful for the treatment of inflammatory bowel diseases (IBDs), including Crohn's disease, as it suppresses the production of relevant MP proinflammatory cytokines. However, because P-ATPase was not detected in MPs, the mechanism is unclear and remains to be studied further in an IBD animal model.

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“…There are still doubts whether vascular lesions would or would not be accompanied by lesions of the intrinsic nervous system of the intestine 11 , especially with regard to the myenteric plexus (Auerbach) and submucous plexus (Meissner), with consequent modification of the intestinal motility. Lesions of the nervous system have been described following ischemia/ reperfusion [12][13][14] , and many substances have been studied with a view to diminishing or avoiding these ischemia/reperfusion lesions 11,[15][16][17] . However, it is not fully known what the characteristics of enteric nervous system lesions are, how they occur, and whether such damage is total or causes alterations to cell populations in the intestinal ganglia.…”

Section: Introductionmentioning

confidence: 99%

Do lesions of the enteric nervous system occur following intestinal ischemia/reperfusion?

et al. 2007

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Purpose:To evaluate tissue lesions, especially those of the intestinal innervation, in an excluded jejunal loop subjected to ischemia and reperfusion in rats. Methods: To evaluate the role of ischemia and reperfusion lesions in an excluded intestinal loop, four groups of 20 rats were set up: control group (GCEI7) and three experimental groups (GIREI7, GIREI14 and GIREI28). They were all subjected to exclusion of an intestinal segment of six centimeters in length, at a distance of 10 centimeters from the Treitz angle. The 60 animals in the three experimental groups were additionally subjected to ischemia of the vascular pedicle for 30 minutes. The control group and the experimental group GIREI7 were evaluated on the 7 th day after the operation. The groups GIREI14 and GIREI28 (which also underwent ischemia) were utilized to evaluate the evolution of the lesion over time, on the 14 th and 28 th days after the operation, respectively. From the intestinal excluded loop, we take one ring of 0,5 cm distal and proximal, that were fixed in formaline 10% solution in order to do histological (HE) and immuno-hystochemial (PS-100) evaluation (enteric nervous system.) The distal loop was exteriorized in stoma and the proximal part closed with polipropilene 6-0. Results: It was observed a decrease in the number of ganglionic cells in the myenteric plexus in the group subjected to ischemia and reperfusion (GIREI7), in relation to the control group (GCEI7) at the 7 th post-operative day (Mann-Whitney test: p = 0.0173 *. Comparing the numbers of ganglionic cells in the myenteric plexus before and after jejunal loop exclusion GCEI7 -(Wilcoxon test: p = 0.0577). GIREI7 -Comparing the numbers of ganglionic cells in the myenteric plexus before and after ischemia (*p = 0.0399). Comparing the percentage variations in ganglionic cells in the myenteric plexus on the 7 th , 14 th and 28 th days after the procedure, in the groups GIREI7, GIREI14 and GIREI28, it was observed that there were no significant alterations. Kruskal-Wallis test: p = 0.6501. Conclusion: There was a decrease in the number of ganglionic cells in the myenteric plexus due to ischemia and reperfusion that did not recover in the late post-operative period. Key words: Intestine, small. Ischemia. Reperfusion. Enteric nervous system. RESUMO Objetivo: Avaliar lesões teciduais, especialmente aquelas da inervação intestinal em alça jejunal excluída submetida à isquemia e reperfusão em ratos. Métodos: Para avaliar o papel da isquemia e reperfusão nas lesões em uma alça intestinal exclusa, quatro grupos de 20 ratos foram criados: Grupo controle (GCE17) e 3 Grupos experimentais (GIRE!7, GIREI14) e GIREI28) Todos foram submetidos à exclusão de um segmento intestinal de seis centímetros de extensão, a 10 centímetros do ângulo de Treitz . Os 60 animais dos 3 grupos experimentais foram também submetidos a isquemia do pedículo vascular por 30 minutos.O grupo controle e o grupo experimental GIREI7 foram avaliados no 7º. Dia após a operação. Os grupos GIREI14 e GIREI28 também ...

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Effects of omeprazole and gentamicin on the biochemical and histopathological alterations of the hypoxia/ reoxygenation induced intestinal injury in newborn rats

Cited by 21 publications

References 33 publications

Protective effects of vitamin E and omeprazole on the hypoxia/reoxygenation induced intestinal injury in newborn rats

Protective effects of vitamin E and omeprazole on the hypoxia/reoxygenation induced intestinal injury in newborn rats

Suppression of proinflammatory cytokine production in macrophages by lansoprazole

Do lesions of the enteric nervous system occur following intestinal ischemia/reperfusion?

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