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Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn(2+)
Tannic acid (TA) is a polyphenolic compound that exerts protective effects under pathological conditions. The diverse mechanisms of TA can exert beneficial anti-oxidative, anti-inflammatory, and anti-cancer effects. Herein, we reported that TA affords robust neuroprotection in an animal model of str...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9423855/ https://www.ncbi.nlm.nih.gov/pubmed/36046027 http://dx.doi.org/10.1080/19768354.2022.2113915 |
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author | Kim, Seung Woo Kim, Da Bin Kim, Hong Seok |
author_facet | Kim, Seung Woo Kim, Da Bin Kim, Hong Seok |
author_sort | Kim, Seung Woo |
collection | PubMed |
description | Tannic acid (TA) is a polyphenolic compound that exerts protective effects under pathological conditions. The diverse mechanisms of TA can exert beneficial anti-oxidative, anti-inflammatory, and anti-cancer effects. Herein, we reported that TA affords robust neuroprotection in an animal model of stroke (transient middle cerebral artery occlusion; tMCAO) and exhibits Zn(2+)-chelating and anti-oxidative effects in primary cortical neurons. Following tMCAO induction, intravenous administration of TA (5 mg/kg) suppressed infarct formation by 32.9 ± 16.2% when compared with tMCAO control animals, improving neurological deficits and motor function. We compared the chelation activity under several ionic conditions and observed that TA showed better Zn(2+) chelation than Cu(2+). Furthermore, TA markedly decreased lactate dehydrogenase release following acute Zn(2+) treatment and subsequently reduced the expression of p67 (a cytosolic component of NADPH oxidase), indicating the potential mechanism underlying TA-mediated Zn(2+) chelation and anti-oxidative effects in primary cortical neurons. These findings suggest that anti-Zn(2+) toxicity and anti-oxidative effects participate in the TA-mediated neuroprotective effects in the postischemic brain. |
format | Online Article Text |
id | pubmed-9423855 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-94238552022-08-30 Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn(2+) Kim, Seung Woo Kim, Da Bin Kim, Hong Seok Anim Cells Syst (Seoul) Neuroscience Tannic acid (TA) is a polyphenolic compound that exerts protective effects under pathological conditions. The diverse mechanisms of TA can exert beneficial anti-oxidative, anti-inflammatory, and anti-cancer effects. Herein, we reported that TA affords robust neuroprotection in an animal model of stroke (transient middle cerebral artery occlusion; tMCAO) and exhibits Zn(2+)-chelating and anti-oxidative effects in primary cortical neurons. Following tMCAO induction, intravenous administration of TA (5 mg/kg) suppressed infarct formation by 32.9 ± 16.2% when compared with tMCAO control animals, improving neurological deficits and motor function. We compared the chelation activity under several ionic conditions and observed that TA showed better Zn(2+) chelation than Cu(2+). Furthermore, TA markedly decreased lactate dehydrogenase release following acute Zn(2+) treatment and subsequently reduced the expression of p67 (a cytosolic component of NADPH oxidase), indicating the potential mechanism underlying TA-mediated Zn(2+) chelation and anti-oxidative effects in primary cortical neurons. These findings suggest that anti-Zn(2+) toxicity and anti-oxidative effects participate in the TA-mediated neuroprotective effects in the postischemic brain. Taylor & Francis 2022-08-19 /pmc/articles/PMC9423855/ /pubmed/36046027 http://dx.doi.org/10.1080/19768354.2022.2113915 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Neuroscience Kim, Seung Woo Kim, Da Bin Kim, Hong Seok Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn(2+) |
title | Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn(2+) |
title_full | Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn(2+) |
title_fullStr | Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn(2+) |
title_full_unstemmed | Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn(2+) |
title_short | Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn(2+) |
title_sort | neuroprotective effects of tannic acid in the postischemic brain via direct chelation of zn(2+) |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9423855/ https://www.ncbi.nlm.nih.gov/pubmed/36046027 http://dx.doi.org/10.1080/19768354.2022.2113915 |
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