Effects of a one-week treatment with acid gastric inhibitors on<i>Helicobacter pylori</i>-infected mice

Maróstica, Marta; Arçari, Demétrius Paiva; Bartchewsky, Waldemar; Trevisan, Miriam Aparecida da Silva; Ribeiro, Marcelo Lima; Pedrazzoli, José; Höehr, Nelci Fenalti; Gambero, Alessandra

doi:10.1080/00365520701514396

Cited by 7 publications

(5 citation statements)

References 36 publications

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“…Helicobacter infection models have been a useful tool for identifying new and improving existing treatment protocols for H. pylori ‐associated GC. Administration of the gastric acid inhibitors Omeprazole and Ranitidine following H. pylori infection was shown to improve the healing of macroscopic inflammatory lesions, indicating that partial acid blockade is effective at reducing disease pathology in mice . The effect of long‐term administration of the anti‐inflammatory drugs Nimesulide (Cox‐2 inhibitor) to H. pylori ‐infected mice that were also challenged with MNU significantly lowered the incidence of gastric tumors, indicating that H. pylori –associated inflammation was responsible for promoting gastric carcinogenesis in this model.…”

Section: Helicobacter Infection Modelssupporting

confidence: 62%

“…The eradication of H. pylori in patients with established chronic infections is challenging. Current treatment strategies are focused on long-term maintenance therapy to prevent infection recurrence and typically include combining acid inhibition with a proton pump inhibitor and at least two 79 The effect of long-term administration of the anti-inflammatory drugs Nimesulide (Cox-2 inhibitor) to H. pylori-infected mice that were also challenged with MNU significantly lowered the incidence of gastric tumors, indicating that H. pylori-associated inflammation was responsible for promoting gastric carcinogenesis in this model. Interestingly, Nimesulide treatment also markedly reduced atrophic gastritis.…”

Section: Helicobacter Infection Modelsmentioning

confidence: 99%

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Mouse models for gastric cancer: Matching models to biological questions

Poh

O’Donoghue

Ernst

et al. 2016

J of Gastro and Hepatol

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Gastric cancer is the third leading cause of cancer‐related mortality worldwide. This is in part due to the asymptomatic nature of the disease, which often results in late‐stage diagnosis, at which point there are limited treatment options. Even when treated successfully, gastric cancer patients have a high risk of tumor recurrence and acquired drug resistance. It is vital to gain a better understanding of the molecular mechanisms underlying gastric cancer pathogenesis to facilitate the design of new‐targeted therapies that may improve patient survival. A number of chemically and genetically engineered mouse models of gastric cancer have provided significant insight into the contribution of genetic and environmental factors to disease onset and progression. This review outlines the strengths and limitations of current mouse models of gastric cancer and their relevance to the pre‐clinical development of new therapeutics.

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Section: Helicobacter Infection Modelssupporting

confidence: 62%

Section: Helicobacter Infection Modelsmentioning

confidence: 99%

Mouse models for gastric cancer: Matching models to biological questions

Poh

O’Donoghue

Ernst

et al. 2016

J of Gastro and Hepatol

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“…This study aimed to determine whether treatment with the P450inducing drug phenobarbital early in life can affect the efficacy of a drug taken later in adult life. Omeprazole is a proton-pump inhibitor commonly used to treat stomach ulcers, gastroesophageal reflux disease, and heartburn (Maróstica et al, 2007). Its action involves blocking the release of acid by proton pumps in the stomach so as to raise the pH of the gastric lumen.…”

Section: Introductionmentioning

confidence: 99%

Phenobarbital Treatment at a Neonatal Age Results in Decreased Efficacy of Omeprazole in Adult Mice

Tien

Piekos

Pope

et al. 2017

Drug Metabolism and Disposition

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Drug-drug interactions (DDIs) occur when the action of one drug interferes with or alters the activity of another drug taken concomitantly. This can lead to decreased drug efficacy or increased toxicity. Because of DDIs, physicians in the clinical practice attempt to avoid potential interactions when multiple drugs are coadministrated; however, there is still a large knowledge gap in understanding how drugs taken in the past can contribute to DDIs in the future. The goal of this study was to investigate the consequence of neonatal drug exposure on efficacy of other drugs administered up through adult life. We selected a mouse model to test phenobarbital exposure at a neonatal age and its impact on efficacy of omeprazole in adult life. The results of our experiment show an observed decrease in omeprazole's ability to raise gastric pH in adult mice that received single or multiple doses of phenobarbital at a neonatal age. This effect may be associated with the permanent induction of cytochrome P450 enzymes in adult liver after neonatal phenobarbital treatment. Our data indicates that DDIs may result from drugs administered in the past in an animal model and should prompt re-evaluation of how DDIs are viewed and how to avoid long-term DDIs in clinical practice.

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“…To the best of our knowledge, this is the first case of a child with MD unsuccessfully treated with ranitidine who recovered fully following the use of omeprazole. We speculate that some additional omeprazole‐related properties, like the antiapoptotic activity (12), could explain this finding.…”

Section: Discussionmentioning

confidence: 77%