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Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection
Eudesmin has been proven to possess anti-inflammatory effects. In the present study, the effects of eudesmin on Helicobacter pylori (H. pylori)-mediated autophagy, apoptosis, immune response and inflammation were determined in human gastric adenocarcinoma (AGS) cells in vitro and in C57BL/6 mice in...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5795382/ https://www.ncbi.nlm.nih.gov/pubmed/29456644 http://dx.doi.org/10.3892/etm.2018.5701 |
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author | Yang, Jai-Sing Wang, Chao-Min Su, Chiu-Hsian Ho, Han-Chen Chang, Chiung-Hung Chou, Chang-Hung Hsu, Yuan-Man |
author_facet | Yang, Jai-Sing Wang, Chao-Min Su, Chiu-Hsian Ho, Han-Chen Chang, Chiung-Hung Chou, Chang-Hung Hsu, Yuan-Man |
author_sort | Yang, Jai-Sing |
collection | PubMed |
description | Eudesmin has been proven to possess anti-inflammatory effects. In the present study, the effects of eudesmin on Helicobacter pylori (H. pylori)-mediated autophagy, apoptosis, immune response and inflammation were determined in human gastric adenocarcinoma (AGS) cells in vitro and in C57BL/6 mice in vivo. Detection of the production of interleukin (IL)-8, IL-1β and immunoglobulin M (IgM) was performed using ELISA. Identification of the activation of apoptosis-associated caspase-3, −8 and −9 proteins, Bcl-2-associated X protein (Bax) and BH3 interacting domain death agonist (Bid) protein, was determined through western blot analysis. Autophagy microtubule-associated protein 1A/1B-light chain 3, isoform B (LC-3B) expression was measured using immunostaining. The results of the present study demonstrated that eudesmin inhibited the growth of H. pylori, with increased inhibition activity against antibiotic resistant strains compared with the reference strain. In addition, H. pylori-induced IL-8 secretion, LC-3B expression and apoptosis-associated protein (caspase-3, −8 and −9, Bax and Bid) activation in AGS cells was suppressed by eudesmin. Furthermore, eudesmin suppressed IL-1β and IgM production in H. pylori-infected C57BL/6 mice in vivo. In conclusion, eudesmin may be developed as a promising therapeutic agent to prevent and/or treat H. pylori-associated gastric inflammation. |
format | Online Article Text |
id | pubmed-5795382 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57953822018-02-16 Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection Yang, Jai-Sing Wang, Chao-Min Su, Chiu-Hsian Ho, Han-Chen Chang, Chiung-Hung Chou, Chang-Hung Hsu, Yuan-Man Exp Ther Med Articles Eudesmin has been proven to possess anti-inflammatory effects. In the present study, the effects of eudesmin on Helicobacter pylori (H. pylori)-mediated autophagy, apoptosis, immune response and inflammation were determined in human gastric adenocarcinoma (AGS) cells in vitro and in C57BL/6 mice in vivo. Detection of the production of interleukin (IL)-8, IL-1β and immunoglobulin M (IgM) was performed using ELISA. Identification of the activation of apoptosis-associated caspase-3, −8 and −9 proteins, Bcl-2-associated X protein (Bax) and BH3 interacting domain death agonist (Bid) protein, was determined through western blot analysis. Autophagy microtubule-associated protein 1A/1B-light chain 3, isoform B (LC-3B) expression was measured using immunostaining. The results of the present study demonstrated that eudesmin inhibited the growth of H. pylori, with increased inhibition activity against antibiotic resistant strains compared with the reference strain. In addition, H. pylori-induced IL-8 secretion, LC-3B expression and apoptosis-associated protein (caspase-3, −8 and −9, Bax and Bid) activation in AGS cells was suppressed by eudesmin. Furthermore, eudesmin suppressed IL-1β and IgM production in H. pylori-infected C57BL/6 mice in vivo. In conclusion, eudesmin may be developed as a promising therapeutic agent to prevent and/or treat H. pylori-associated gastric inflammation. D.A. Spandidos 2018-03 2018-01-04 /pmc/articles/PMC5795382/ /pubmed/29456644 http://dx.doi.org/10.3892/etm.2018.5701 Text en Copyright: © Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Yang, Jai-Sing Wang, Chao-Min Su, Chiu-Hsian Ho, Han-Chen Chang, Chiung-Hung Chou, Chang-Hung Hsu, Yuan-Man Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection |
title | Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection |
title_full | Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection |
title_fullStr | Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection |
title_full_unstemmed | Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection |
title_short | Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection |
title_sort | eudesmin attenuates helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of h. pylori infection |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5795382/ https://www.ncbi.nlm.nih.gov/pubmed/29456644 http://dx.doi.org/10.3892/etm.2018.5701 |
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