Cargando…
Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine
OBJECTIVES: To investigate if oral omeprazole application induces cancers of fore and glandular stomach in mice. METHODS: A total of 66 eligible male mice were randomly divided into 6 groups, which were treated with control reagent, low (6 mg/kg) and high dose omeprazole (30 mg/kg), N-methyl-N’-nitr...
Autores principales: | , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5642558/ https://www.ncbi.nlm.nih.gov/pubmed/29050283 http://dx.doi.org/10.18632/oncotarget.19696 |
_version_ | 1783271390150918144 |
---|---|
author | Huang, Lei Qi, Dong-Jiang He, Wei Xu, A-Man |
author_facet | Huang, Lei Qi, Dong-Jiang He, Wei Xu, A-Man |
author_sort | Huang, Lei |
collection | PubMed |
description | OBJECTIVES: To investigate if oral omeprazole application induces cancers of fore and glandular stomach in mice. METHODS: A total of 66 eligible male mice were randomly divided into 6 groups, which were treated with control reagent, low (6 mg/kg) and high dose omeprazole (30 mg/kg), N-methyl-N’-nitro-N-nitrosoguanidine (MNNG, 100 mg/L water), and MNNG plus low and high dose omeprazole, respectively. After 24 weeks, concentrations of acid phosphatase (ACP) and N-acetyl-β-D-glucosaminidase(NAG) in serum and spleen was examined, and p21 and mTOR levels in stomach were detected. RESULTS: The mouse spleen weight index was smaller in the omeprazole group than the control group, and in the MNNG plus omeprazole groups than the MNNG group. In the fore-stomach, more carcinomas were observed in the MNNG plus omeprazole groups than in the MNNG group. In the glandular stomach, there existed more atypical hyperplasia cases in the MNNG plus omeprazole groups than the MNNG-treated group, and one carcinoma was induced in the MNNG plus high dose omeprazole group. Omeprazole alone caused minor gastric pathological changes. Omeprazole treatment lowered both serum and spleen ACP and NAG levels in both the non-MNNG-treated and MNNG-treated subgroups. In fore-stomach, there existed decreased p21 and mTOR levels in the omeprazole-treated groups than in the control group, and in the MNNG plus omeprazole groups than the MNNG-treated group. CONCLUSION: Omeprazole promotes carcinogenesis of the mouse fore-stomach but not the glandular stomach following treatment with MNNG. Lysosomal hydrolase activity was inhibited and some cancer-associated proteins was dysregulated, which requires further explorations. |
format | Online Article Text |
id | pubmed-5642558 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-56425582017-10-18 Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine Huang, Lei Qi, Dong-Jiang He, Wei Xu, A-Man Oncotarget Research Paper OBJECTIVES: To investigate if oral omeprazole application induces cancers of fore and glandular stomach in mice. METHODS: A total of 66 eligible male mice were randomly divided into 6 groups, which were treated with control reagent, low (6 mg/kg) and high dose omeprazole (30 mg/kg), N-methyl-N’-nitro-N-nitrosoguanidine (MNNG, 100 mg/L water), and MNNG plus low and high dose omeprazole, respectively. After 24 weeks, concentrations of acid phosphatase (ACP) and N-acetyl-β-D-glucosaminidase(NAG) in serum and spleen was examined, and p21 and mTOR levels in stomach were detected. RESULTS: The mouse spleen weight index was smaller in the omeprazole group than the control group, and in the MNNG plus omeprazole groups than the MNNG group. In the fore-stomach, more carcinomas were observed in the MNNG plus omeprazole groups than in the MNNG group. In the glandular stomach, there existed more atypical hyperplasia cases in the MNNG plus omeprazole groups than the MNNG-treated group, and one carcinoma was induced in the MNNG plus high dose omeprazole group. Omeprazole alone caused minor gastric pathological changes. Omeprazole treatment lowered both serum and spleen ACP and NAG levels in both the non-MNNG-treated and MNNG-treated subgroups. In fore-stomach, there existed decreased p21 and mTOR levels in the omeprazole-treated groups than in the control group, and in the MNNG plus omeprazole groups than the MNNG-treated group. CONCLUSION: Omeprazole promotes carcinogenesis of the mouse fore-stomach but not the glandular stomach following treatment with MNNG. Lysosomal hydrolase activity was inhibited and some cancer-associated proteins was dysregulated, which requires further explorations. Impact Journals LLC 2017-07-31 /pmc/articles/PMC5642558/ /pubmed/29050283 http://dx.doi.org/10.18632/oncotarget.19696 Text en Copyright: © 2017 Huang et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Huang, Lei Qi, Dong-Jiang He, Wei Xu, A-Man Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine |
title | Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine |
title_full | Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine |
title_fullStr | Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine |
title_full_unstemmed | Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine |
title_short | Omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine |
title_sort | omeprazole promotes carcinogenesis of fore-stomach in mice with co-stimulation of nitrosamine |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5642558/ https://www.ncbi.nlm.nih.gov/pubmed/29050283 http://dx.doi.org/10.18632/oncotarget.19696 |
work_keys_str_mv | AT huanglei omeprazolepromotescarcinogenesisofforestomachinmicewithcostimulationofnitrosamine AT qidongjiang omeprazolepromotescarcinogenesisofforestomachinmicewithcostimulationofnitrosamine AT hewei omeprazolepromotescarcinogenesisofforestomachinmicewithcostimulationofnitrosamine AT xuaman omeprazolepromotescarcinogenesisofforestomachinmicewithcostimulationofnitrosamine |