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NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1)

BACKGROUND: Both H. pylori infection and high salt (NaCl) diet are risks of gastric cancer, however, the interaction pattern of the two is not very clear. Our objective was to investigate the effects of NaCl-pretreated H. pylori on DNA damage and proliferation of gastric epithelial cell (GES-1). MET...

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Autores principales: Xu, Ying, Yan, Ying, Hou, Ming-xiao, Liu, Yun-en
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391598/
https://www.ncbi.nlm.nih.gov/pubmed/25859277
http://dx.doi.org/10.1186/s13027-015-0003-3
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author Xu, Ying
Yan, Ying
Hou, Ming-xiao
Liu, Yun-en
author_facet Xu, Ying
Yan, Ying
Hou, Ming-xiao
Liu, Yun-en
author_sort Xu, Ying
collection PubMed
description BACKGROUND: Both H. pylori infection and high salt (NaCl) diet are risks of gastric cancer, however, the interaction pattern of the two is not very clear. Our objective was to investigate the effects of NaCl-pretreated H. pylori on DNA damage and proliferation of gastric epithelial cell (GES-1). METHODS: GES-1 cells were co-cultured with H.pylori or NaCl-pretreated H. pylori (with 30% NaCl) for 24 h. The morphological changes of all cells were observed by inverted phase contrast microscopy and transmission electron microscopy. Oxidative DNA damage was examined by immunofluorescence. Alterations in mitochondrial membrane potential and apoptosis rate were detected by flow cytometry and western blot, and expression of Ki-67, PCNA and P21 were evaluated using the immunocytochemical staining. RESULTS: GES-1 cells co-cultured with NaCl-pretreated H.pylori exhibited morphological changes and oxidative DNA damage. Although no significant disruption of the mitochondrial membrane potential (ΔΨm) and apoptotic rate were observed compared with control groups, there were significant decreased in Bax and Caspase3 proteins and increased in Bcl-2 protein in GES-1 cells infected with H. pylori(30) when compared with GES-1 cells cultured with H. pylori. In addition, we found a proliferative effect on GES-1 cells with an increased expression of Ki-67 and PCNA as well as a decreased p21 expression, through which the cells may acquire the potential for malignant transformation. CONCLUSION: NaCl-pretreated H. pylori possessed the ability to cause cell injury and promote proliferation in gastric epithelial cells.
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spelling pubmed-43915982015-04-10 NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1) Xu, Ying Yan, Ying Hou, Ming-xiao Liu, Yun-en Infect Agent Cancer Research Article BACKGROUND: Both H. pylori infection and high salt (NaCl) diet are risks of gastric cancer, however, the interaction pattern of the two is not very clear. Our objective was to investigate the effects of NaCl-pretreated H. pylori on DNA damage and proliferation of gastric epithelial cell (GES-1). METHODS: GES-1 cells were co-cultured with H.pylori or NaCl-pretreated H. pylori (with 30% NaCl) for 24 h. The morphological changes of all cells were observed by inverted phase contrast microscopy and transmission electron microscopy. Oxidative DNA damage was examined by immunofluorescence. Alterations in mitochondrial membrane potential and apoptosis rate were detected by flow cytometry and western blot, and expression of Ki-67, PCNA and P21 were evaluated using the immunocytochemical staining. RESULTS: GES-1 cells co-cultured with NaCl-pretreated H.pylori exhibited morphological changes and oxidative DNA damage. Although no significant disruption of the mitochondrial membrane potential (ΔΨm) and apoptotic rate were observed compared with control groups, there were significant decreased in Bax and Caspase3 proteins and increased in Bcl-2 protein in GES-1 cells infected with H. pylori(30) when compared with GES-1 cells cultured with H. pylori. In addition, we found a proliferative effect on GES-1 cells with an increased expression of Ki-67 and PCNA as well as a decreased p21 expression, through which the cells may acquire the potential for malignant transformation. CONCLUSION: NaCl-pretreated H. pylori possessed the ability to cause cell injury and promote proliferation in gastric epithelial cells. BioMed Central 2015-03-01 /pmc/articles/PMC4391598/ /pubmed/25859277 http://dx.doi.org/10.1186/s13027-015-0003-3 Text en © Xu et al; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Xu, Ying
Yan, Ying
Hou, Ming-xiao
Liu, Yun-en
NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1)
title NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1)
title_full NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1)
title_fullStr NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1)
title_full_unstemmed NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1)
title_short NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1)
title_sort nacl pretreatment attenuates h.pylori-induced dna damage and exacerbates proliferation of gastric epithelial cells (ges-1)
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391598/
https://www.ncbi.nlm.nih.gov/pubmed/25859277
http://dx.doi.org/10.1186/s13027-015-0003-3
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