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The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy
Radiocontrast-induced nephropathy (CIN) is the third most common cause of acute renal failure. The pathophysiology of CIN is related to tubular injury caused by oxidative stress, and nuclear factor erythroid-2-related factor 2 (Nrf2) is critical in coordinating intracellular antioxidative processes....
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6384919/ https://www.ncbi.nlm.nih.gov/pubmed/30796317 http://dx.doi.org/10.1038/s41598-019-39534-2 |
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author | Kim, Ji Eun Bae, So Yeon Ahn, Shin Young Kwon, Young Joo Ko, Gang Jee |
author_facet | Kim, Ji Eun Bae, So Yeon Ahn, Shin Young Kwon, Young Joo Ko, Gang Jee |
author_sort | Kim, Ji Eun |
collection | PubMed |
description | Radiocontrast-induced nephropathy (CIN) is the third most common cause of acute renal failure. The pathophysiology of CIN is related to tubular injury caused by oxidative stress, and nuclear factor erythroid-2-related factor 2 (Nrf2) is critical in coordinating intracellular antioxidative processes. We thus investigated the role of Nrf2 in CIN. CIN was established in mice and in NRK-52E cells via iohexol administration according to the protocols of previous studies. To determine the role of Nrf2 in CIN, Nrf2 expression was reduced in vivo using Nrf2 knockout (KO) mice (B6.129 × 1-Nfe2 l2tm1Ywk/J) and in vitro with siRNA treatment targeting Nrf2. Increased Nrf2 expression was observed after iohexol treatment both in vivo and in vitro. Serum creatinine at 24 h after iohexol injection was significantly higher in KO mice than in wild-type (WT) mice. Histologic examination showed that iohexol-induced tubular vacuolization and structural disruption were aggravated in Nrf2 KO mice. Significant increases in apoptosis and F4/80(+) inflammatory cell infiltration were demonstrated in KO mice compared to WT mice. In addition, the increase in reactive oxygen species after iohexol treatment was augmented by Nrf2 inhibition both in vivo and in vitro. Nrf2 may be implicated in the pathogenesis of CIN via the modulation of antioxidant, anti-apoptotic, and anti-inflammatory processes. |
format | Online Article Text |
id | pubmed-6384919 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-63849192019-02-26 The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy Kim, Ji Eun Bae, So Yeon Ahn, Shin Young Kwon, Young Joo Ko, Gang Jee Sci Rep Article Radiocontrast-induced nephropathy (CIN) is the third most common cause of acute renal failure. The pathophysiology of CIN is related to tubular injury caused by oxidative stress, and nuclear factor erythroid-2-related factor 2 (Nrf2) is critical in coordinating intracellular antioxidative processes. We thus investigated the role of Nrf2 in CIN. CIN was established in mice and in NRK-52E cells via iohexol administration according to the protocols of previous studies. To determine the role of Nrf2 in CIN, Nrf2 expression was reduced in vivo using Nrf2 knockout (KO) mice (B6.129 × 1-Nfe2 l2tm1Ywk/J) and in vitro with siRNA treatment targeting Nrf2. Increased Nrf2 expression was observed after iohexol treatment both in vivo and in vitro. Serum creatinine at 24 h after iohexol injection was significantly higher in KO mice than in wild-type (WT) mice. Histologic examination showed that iohexol-induced tubular vacuolization and structural disruption were aggravated in Nrf2 KO mice. Significant increases in apoptosis and F4/80(+) inflammatory cell infiltration were demonstrated in KO mice compared to WT mice. In addition, the increase in reactive oxygen species after iohexol treatment was augmented by Nrf2 inhibition both in vivo and in vitro. Nrf2 may be implicated in the pathogenesis of CIN via the modulation of antioxidant, anti-apoptotic, and anti-inflammatory processes. Nature Publishing Group UK 2019-02-22 /pmc/articles/PMC6384919/ /pubmed/30796317 http://dx.doi.org/10.1038/s41598-019-39534-2 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Kim, Ji Eun Bae, So Yeon Ahn, Shin Young Kwon, Young Joo Ko, Gang Jee The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy |
title | The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy |
title_full | The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy |
title_fullStr | The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy |
title_full_unstemmed | The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy |
title_short | The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy |
title_sort | role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6384919/ https://www.ncbi.nlm.nih.gov/pubmed/30796317 http://dx.doi.org/10.1038/s41598-019-39534-2 |
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