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Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study
To explore the protective role of hydrogen gas (H(2)) on oxidative damage and apoptosis in intestinal porcine epithelial cells (IPEC-J2) induced by deoxynivalenol (DON), cells were assigned to four treatment groups, including control, 5 μM DON, H(2)-saturated medium, and 5 μM DON + H(2)-saturated me...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020398/ https://www.ncbi.nlm.nih.gov/pubmed/31861743 http://dx.doi.org/10.3390/toxins12010005 |
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author | Ji, Xu Zheng, Weijiang Yao, Wen |
author_facet | Ji, Xu Zheng, Weijiang Yao, Wen |
author_sort | Ji, Xu |
collection | PubMed |
description | To explore the protective role of hydrogen gas (H(2)) on oxidative damage and apoptosis in intestinal porcine epithelial cells (IPEC-J2) induced by deoxynivalenol (DON), cells were assigned to four treatment groups, including control, 5 μM DON, H(2)-saturated medium, and 5 μM DON + H(2)-saturated medium treatments. After 12 h of different treatments, the cell viability, biomarkers of cell redox states, and gene expression of antioxidant enzymes and apoptosis were observed and detected. Furthermore, caspase-3 and Bax protein expressions were measured by Western blot analysis. Our results demonstrated that the 5 μM DON significantly caused cytotoxicity to IPEC-J2 cells by reducing cell viability and increasing lactate dehydrogenase release in culture supernatants. Moreover, DON treatments significantly increased levels of 8-hydroxy-2′-deoxyguanosine, 3-nitrotyrosine, and malonaldehyde; however, they decreased total superoxide dismutase and catalase activities and downregulated messenger RNA (mRNA) expression related to antioxidant enzymes in cells. The 5 μM DON treatment also downregulated Bcl-2 expression and upregulated caspase-3 and Bax expression. However, the H(2)-saturated medium significantly improved cell growth status and reversed the change of redox states and expression of genes and proteins related to apoptosis induced by DON in IPEC-J2 cells. In conclusion, H(2) could protect IPEC-J2 cells from DON-induced oxidative damage and apoptosis in vitro. |
format | Online Article Text |
id | pubmed-7020398 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-70203982020-03-09 Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study Ji, Xu Zheng, Weijiang Yao, Wen Toxins (Basel) Communication To explore the protective role of hydrogen gas (H(2)) on oxidative damage and apoptosis in intestinal porcine epithelial cells (IPEC-J2) induced by deoxynivalenol (DON), cells were assigned to four treatment groups, including control, 5 μM DON, H(2)-saturated medium, and 5 μM DON + H(2)-saturated medium treatments. After 12 h of different treatments, the cell viability, biomarkers of cell redox states, and gene expression of antioxidant enzymes and apoptosis were observed and detected. Furthermore, caspase-3 and Bax protein expressions were measured by Western blot analysis. Our results demonstrated that the 5 μM DON significantly caused cytotoxicity to IPEC-J2 cells by reducing cell viability and increasing lactate dehydrogenase release in culture supernatants. Moreover, DON treatments significantly increased levels of 8-hydroxy-2′-deoxyguanosine, 3-nitrotyrosine, and malonaldehyde; however, they decreased total superoxide dismutase and catalase activities and downregulated messenger RNA (mRNA) expression related to antioxidant enzymes in cells. The 5 μM DON treatment also downregulated Bcl-2 expression and upregulated caspase-3 and Bax expression. However, the H(2)-saturated medium significantly improved cell growth status and reversed the change of redox states and expression of genes and proteins related to apoptosis induced by DON in IPEC-J2 cells. In conclusion, H(2) could protect IPEC-J2 cells from DON-induced oxidative damage and apoptosis in vitro. MDPI 2019-12-19 /pmc/articles/PMC7020398/ /pubmed/31861743 http://dx.doi.org/10.3390/toxins12010005 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Communication Ji, Xu Zheng, Weijiang Yao, Wen Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study |
title | Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study |
title_full | Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study |
title_fullStr | Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study |
title_full_unstemmed | Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study |
title_short | Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study |
title_sort | protective role of hydrogen gas on oxidative damage and apoptosis in intestinal porcine epithelial cells (ipec-j2) induced by deoxynivalenol: a preliminary study |
topic | Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020398/ https://www.ncbi.nlm.nih.gov/pubmed/31861743 http://dx.doi.org/10.3390/toxins12010005 |
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