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Sulforaphane prevents PC12 cells from oxidative damage via the Nrf2 pathway
The aim of this study was to investigate the protective effect of sulforaphane (SFN) on 1-methyl-4-phenyl pyridine ion (MPP+)-induced cytotoxicity and to investigate its possible mechanisms. Methods: PC12 cell toxicity induced by MPP+ served as a cell model of Parkinson's diseases. The cell cul...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6522909/ https://www.ncbi.nlm.nih.gov/pubmed/31059012 http://dx.doi.org/10.3892/mmr.2019.10148 |
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author | Bao, Bing Zhang, Man-Qing Chen, Zhi-Ying Wu, Xiang-Bing Xia, Zhong-Bing Chai, Jing-Yan Yin, Xiao-Ping |
author_facet | Bao, Bing Zhang, Man-Qing Chen, Zhi-Ying Wu, Xiang-Bing Xia, Zhong-Bing Chai, Jing-Yan Yin, Xiao-Ping |
author_sort | Bao, Bing |
collection | PubMed |
description | The aim of this study was to investigate the protective effect of sulforaphane (SFN) on 1-methyl-4-phenyl pyridine ion (MPP+)-induced cytotoxicity and to investigate its possible mechanisms. Methods: PC12 cell toxicity induced by MPP+ served as a cell model of Parkinson's diseases. The cell culture + experiments were divided into four groups based on the different treatments, namely, vehicle control, SFN, MPP+ and SFN pretreatment plus MPP+. Cell viability and apoptosis were examined by MTT assay and flow cytometry, respectively. Expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1) and nicotinamide quinone oxidoreductase 1 (NQO1) were detected using western blotting. Results: MPP+ reduced the survival rate of PC12 cells in a dose- and time-dependent manner. After 24-h treatment with 500 µmol/l MPP+, the survival rate of PC12 cells decreased to 58.2±0.03% of that in the control groups. Under the same conditions MPP+ resulted in significant apoptosis of PC12 cells (apoptosis rate: 30.4±0.6%). However, SFN pretreatment significantly attenuated the cell damage induced by MPP+. Furthermore, it was demonstrated that SFN reversed the reduction of Nrf2, HO-1 and NQO1 expression induced by MPP+. Conclusion: SFN may protect PC12 cells from MPP+-induced damage via activating the Nrf2-ARE (antioxidant responsive element) pathway. |
format | Online Article Text |
id | pubmed-6522909 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-65229092019-06-18 Sulforaphane prevents PC12 cells from oxidative damage via the Nrf2 pathway Bao, Bing Zhang, Man-Qing Chen, Zhi-Ying Wu, Xiang-Bing Xia, Zhong-Bing Chai, Jing-Yan Yin, Xiao-Ping Mol Med Rep Articles The aim of this study was to investigate the protective effect of sulforaphane (SFN) on 1-methyl-4-phenyl pyridine ion (MPP+)-induced cytotoxicity and to investigate its possible mechanisms. Methods: PC12 cell toxicity induced by MPP+ served as a cell model of Parkinson's diseases. The cell culture + experiments were divided into four groups based on the different treatments, namely, vehicle control, SFN, MPP+ and SFN pretreatment plus MPP+. Cell viability and apoptosis were examined by MTT assay and flow cytometry, respectively. Expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1) and nicotinamide quinone oxidoreductase 1 (NQO1) were detected using western blotting. Results: MPP+ reduced the survival rate of PC12 cells in a dose- and time-dependent manner. After 24-h treatment with 500 µmol/l MPP+, the survival rate of PC12 cells decreased to 58.2±0.03% of that in the control groups. Under the same conditions MPP+ resulted in significant apoptosis of PC12 cells (apoptosis rate: 30.4±0.6%). However, SFN pretreatment significantly attenuated the cell damage induced by MPP+. Furthermore, it was demonstrated that SFN reversed the reduction of Nrf2, HO-1 and NQO1 expression induced by MPP+. Conclusion: SFN may protect PC12 cells from MPP+-induced damage via activating the Nrf2-ARE (antioxidant responsive element) pathway. D.A. Spandidos 2019-06 2019-04-10 /pmc/articles/PMC6522909/ /pubmed/31059012 http://dx.doi.org/10.3892/mmr.2019.10148 Text en Copyright: © Bao 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 Bao, Bing Zhang, Man-Qing Chen, Zhi-Ying Wu, Xiang-Bing Xia, Zhong-Bing Chai, Jing-Yan Yin, Xiao-Ping Sulforaphane prevents PC12 cells from oxidative damage via the Nrf2 pathway |
title | Sulforaphane prevents PC12 cells from oxidative damage via the Nrf2 pathway |
title_full | Sulforaphane prevents PC12 cells from oxidative damage via the Nrf2 pathway |
title_fullStr | Sulforaphane prevents PC12 cells from oxidative damage via the Nrf2 pathway |
title_full_unstemmed | Sulforaphane prevents PC12 cells from oxidative damage via the Nrf2 pathway |
title_short | Sulforaphane prevents PC12 cells from oxidative damage via the Nrf2 pathway |
title_sort | sulforaphane prevents pc12 cells from oxidative damage via the nrf2 pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6522909/ https://www.ncbi.nlm.nih.gov/pubmed/31059012 http://dx.doi.org/10.3892/mmr.2019.10148 |
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