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Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation
Aristolochic acid (AA) is a component identified in traditional Chinese remedies for the treatment of arthritic pain, coughs and gastrointestinal symptoms. However, previous studies have indicated that AA can induce oxidative stress in renal cells leading to nephropathy. α-tocopherol exists in numer...
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/PMC5780138/ https://www.ncbi.nlm.nih.gov/pubmed/29115579 http://dx.doi.org/10.3892/mmr.2017.7921 |
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author | Wu, Tsai-Kun Pan, Ying-Ru Wang, Hsueh-Fang Wei, Chyou-Wei Yu, Yung-Luen |
author_facet | Wu, Tsai-Kun Pan, Ying-Ru Wang, Hsueh-Fang Wei, Chyou-Wei Yu, Yung-Luen |
author_sort | Wu, Tsai-Kun |
collection | PubMed |
description | Aristolochic acid (AA) is a component identified in traditional Chinese remedies for the treatment of arthritic pain, coughs and gastrointestinal symptoms. However, previous studies have indicated that AA can induce oxidative stress in renal cells leading to nephropathy. α-tocopherol exists in numerous types of food, such as nuts, and belongs to the vitamin E isoform family. It possesses antioxidant activities and has been used previously for clinical applications. Therefore, the aim of the present study was to determine whether α-tocopherol could reduce AA-induced oxidative stress and renal cell cytotoxicity, determined by cell survival rate, reactive oxygen species detection and apoptotic features. The results indicated that AA markedly induced H(2)O(2) levels and caspase-3 activity in renal tubular epithelial cells. Notably, the presence of α-tocopherol inhibited AA-induced H(2)O(2) and caspase-3 activity. The present study demonstrated that antioxidant mechanisms of α-tocopherol may be involved in the increased survival rates from AA-induced cell injury. |
format | Online Article Text |
id | pubmed-5780138 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57801382018-02-05 Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation Wu, Tsai-Kun Pan, Ying-Ru Wang, Hsueh-Fang Wei, Chyou-Wei Yu, Yung-Luen Mol Med Rep Articles Aristolochic acid (AA) is a component identified in traditional Chinese remedies for the treatment of arthritic pain, coughs and gastrointestinal symptoms. However, previous studies have indicated that AA can induce oxidative stress in renal cells leading to nephropathy. α-tocopherol exists in numerous types of food, such as nuts, and belongs to the vitamin E isoform family. It possesses antioxidant activities and has been used previously for clinical applications. Therefore, the aim of the present study was to determine whether α-tocopherol could reduce AA-induced oxidative stress and renal cell cytotoxicity, determined by cell survival rate, reactive oxygen species detection and apoptotic features. The results indicated that AA markedly induced H(2)O(2) levels and caspase-3 activity in renal tubular epithelial cells. Notably, the presence of α-tocopherol inhibited AA-induced H(2)O(2) and caspase-3 activity. The present study demonstrated that antioxidant mechanisms of α-tocopherol may be involved in the increased survival rates from AA-induced cell injury. D.A. Spandidos 2018-01 2017-10-27 /pmc/articles/PMC5780138/ /pubmed/29115579 http://dx.doi.org/10.3892/mmr.2017.7921 Text en Copyright: © Wu 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 Wu, Tsai-Kun Pan, Ying-Ru Wang, Hsueh-Fang Wei, Chyou-Wei Yu, Yung-Luen Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation |
title | Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation |
title_full | Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation |
title_fullStr | Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation |
title_full_unstemmed | Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation |
title_short | Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation |
title_sort | vitamin e (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5780138/ https://www.ncbi.nlm.nih.gov/pubmed/29115579 http://dx.doi.org/10.3892/mmr.2017.7921 |
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