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Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation
BACKGROUND: Isoflavones are biologically active compounds that occur naturally in a variety of plants, with relatively high levels in soybean. Tectorigenin, an isoflavone, protects against hydrogen peroxide (H(2)O(2))-induced cell damage. However, the underlying mechanism is unknown. METHODS: The MT...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Society of Cancer Prevention
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207610/ https://www.ncbi.nlm.nih.gov/pubmed/28053960 http://dx.doi.org/10.15430/JCP.2016.21.4.257 |
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author | Zhang, Rui Piao, Mei Jing Oh, Min Chang Park, Jeong Eon Shilnikova, Kristina Moon, Yu Jin Kim, Dong Hyun Jung, Uhee Kim, In Gyu Hyun, Jin Won |
author_facet | Zhang, Rui Piao, Mei Jing Oh, Min Chang Park, Jeong Eon Shilnikova, Kristina Moon, Yu Jin Kim, Dong Hyun Jung, Uhee Kim, In Gyu Hyun, Jin Won |
author_sort | Zhang, Rui |
collection | PubMed |
description | BACKGROUND: Isoflavones are biologically active compounds that occur naturally in a variety of plants, with relatively high levels in soybean. Tectorigenin, an isoflavone, protects against hydrogen peroxide (H(2)O(2))-induced cell damage. However, the underlying mechanism is unknown. METHODS: The MTT assay was performed to determine cell viability. Catalase activity was assessed by determining the amount of enzyme required to degrade 1 μM H(2)O(2). Protein expression of catalase, phospho-extracellular signal-regulated kinase (ERK), IκB-α, and NF-κB were evaluated by Western blot analysis. A mobility shift assay was performed to assess the DNA-binding ability of NF-κB. Transient transfection and a NF-κB luciferase assay were performed to assess transcriptional activity. RESULTS: Tectorigenin reduced H(2)O(2)-induced death of Chinese hamster lung fibroblasts (V79-4). In addition, tectorigenin increased the activity and protein expression of catalase. Blockade of catalase activity attenuated the protective effect of tectorigenin against oxidative stress. Furthermore, tectorigenin enhanced phosphorylation of ERK and nuclear expression of NF-κB, while inhibition of ERK and NF-κB attenuated the protective effect of tectorigenin against oxidative stress. CONCLUSIONS: Tectorigenin protects cells against oxidative damage by activating catalase and modulating the ERK and NF-κB signaling pathway. |
format | Online Article Text |
id | pubmed-5207610 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Korean Society of Cancer Prevention |
record_format | MEDLINE/PubMed |
spelling | pubmed-52076102017-01-04 Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation Zhang, Rui Piao, Mei Jing Oh, Min Chang Park, Jeong Eon Shilnikova, Kristina Moon, Yu Jin Kim, Dong Hyun Jung, Uhee Kim, In Gyu Hyun, Jin Won J Cancer Prev Original Article BACKGROUND: Isoflavones are biologically active compounds that occur naturally in a variety of plants, with relatively high levels in soybean. Tectorigenin, an isoflavone, protects against hydrogen peroxide (H(2)O(2))-induced cell damage. However, the underlying mechanism is unknown. METHODS: The MTT assay was performed to determine cell viability. Catalase activity was assessed by determining the amount of enzyme required to degrade 1 μM H(2)O(2). Protein expression of catalase, phospho-extracellular signal-regulated kinase (ERK), IκB-α, and NF-κB were evaluated by Western blot analysis. A mobility shift assay was performed to assess the DNA-binding ability of NF-κB. Transient transfection and a NF-κB luciferase assay were performed to assess transcriptional activity. RESULTS: Tectorigenin reduced H(2)O(2)-induced death of Chinese hamster lung fibroblasts (V79-4). In addition, tectorigenin increased the activity and protein expression of catalase. Blockade of catalase activity attenuated the protective effect of tectorigenin against oxidative stress. Furthermore, tectorigenin enhanced phosphorylation of ERK and nuclear expression of NF-κB, while inhibition of ERK and NF-κB attenuated the protective effect of tectorigenin against oxidative stress. CONCLUSIONS: Tectorigenin protects cells against oxidative damage by activating catalase and modulating the ERK and NF-κB signaling pathway. Korean Society of Cancer Prevention 2016-12 2016-12-30 /pmc/articles/PMC5207610/ /pubmed/28053960 http://dx.doi.org/10.15430/JCP.2016.21.4.257 Text en Copyright © 2016 Korean Society of Cancer Prevention This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Zhang, Rui Piao, Mei Jing Oh, Min Chang Park, Jeong Eon Shilnikova, Kristina Moon, Yu Jin Kim, Dong Hyun Jung, Uhee Kim, In Gyu Hyun, Jin Won Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation |
title | Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation |
title_full | Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation |
title_fullStr | Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation |
title_full_unstemmed | Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation |
title_short | Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation |
title_sort | protective effect of an isoflavone, tectorigenin, against oxidative stress-induced cell death via catalase activation |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207610/ https://www.ncbi.nlm.nih.gov/pubmed/28053960 http://dx.doi.org/10.15430/JCP.2016.21.4.257 |
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