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(−)Epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression

(−)Epigallocatechin-3-gallate (EGCG) is a type of polyphenol monomer and is the predominant component of catechin compounds extractable from green tea. Previous studies have demonstrated that EGCG exhibits numerous bioactivities both in vitro and in vivo, including antitumor, antioxidant and anti-in...

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Autores principales: Ding, Li, Gao, Xiang, Hu, Jianlei, Yu, Shenghui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236261/
https://www.ncbi.nlm.nih.gov/pubmed/30320383
http://dx.doi.org/10.3892/mmr.2018.9548
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author Ding, Li
Gao, Xiang
Hu, Jianlei
Yu, Shenghui
author_facet Ding, Li
Gao, Xiang
Hu, Jianlei
Yu, Shenghui
author_sort Ding, Li
collection PubMed
description (−)Epigallocatechin-3-gallate (EGCG) is a type of polyphenol monomer and is the predominant component of catechin compounds extractable from green tea. Previous studies have demonstrated that EGCG exhibits numerous bioactivities both in vitro and in vivo, including antitumor, antioxidant and anti-inflammatory activities, as well as lowering blood lipid levels and protecting against radiation. The present study aimed to investigate whether administration of EGCG may attenuate anesthesia-induced memory deficit in young mice and to reveal the associated underlying mechanisms. The present study revealed that EGCG administration significantly attenuated memory deficit, oxidative stress and cell apoptosis exhibited by anesthesia-induced mice, as determined by Morris water maze testing and ELISA analysis. Furthermore, the results of ELISA and western blot analysis demonstrated that EGCG administration restored acetylcholinesterase activity and modulated the expression levels of neuronal nitric oxide synthase (nNOS), β-amyloid and amyloid precursor protein in anesthesia-induced mice. The present study also employed L-arginine as an nNOS substrate and 7-nitroindazole as an nNOS inhibitor, which were demonstrated to inhibit or potentiate the effects of EGCG, respectively, on anesthesia-induced memory deficit in mice. Therefore, the present study demonstrated that the administration of EGCG attenuated anesthesia-induced memory deficit in young mice, potentially via the modulation of nitric oxide expression and oxidative stress.
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spelling pubmed-62362612018-11-19 (−)Epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression Ding, Li Gao, Xiang Hu, Jianlei Yu, Shenghui Mol Med Rep Articles (−)Epigallocatechin-3-gallate (EGCG) is a type of polyphenol monomer and is the predominant component of catechin compounds extractable from green tea. Previous studies have demonstrated that EGCG exhibits numerous bioactivities both in vitro and in vivo, including antitumor, antioxidant and anti-inflammatory activities, as well as lowering blood lipid levels and protecting against radiation. The present study aimed to investigate whether administration of EGCG may attenuate anesthesia-induced memory deficit in young mice and to reveal the associated underlying mechanisms. The present study revealed that EGCG administration significantly attenuated memory deficit, oxidative stress and cell apoptosis exhibited by anesthesia-induced mice, as determined by Morris water maze testing and ELISA analysis. Furthermore, the results of ELISA and western blot analysis demonstrated that EGCG administration restored acetylcholinesterase activity and modulated the expression levels of neuronal nitric oxide synthase (nNOS), β-amyloid and amyloid precursor protein in anesthesia-induced mice. The present study also employed L-arginine as an nNOS substrate and 7-nitroindazole as an nNOS inhibitor, which were demonstrated to inhibit or potentiate the effects of EGCG, respectively, on anesthesia-induced memory deficit in mice. Therefore, the present study demonstrated that the administration of EGCG attenuated anesthesia-induced memory deficit in young mice, potentially via the modulation of nitric oxide expression and oxidative stress. D.A. Spandidos 2018-12 2018-10-10 /pmc/articles/PMC6236261/ /pubmed/30320383 http://dx.doi.org/10.3892/mmr.2018.9548 Text en Copyright: © Ding 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
Ding, Li
Gao, Xiang
Hu, Jianlei
Yu, Shenghui
(−)Epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression
title (−)Epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression
title_full (−)Epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression
title_fullStr (−)Epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression
title_full_unstemmed (−)Epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression
title_short (−)Epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression
title_sort (−)epigallocatechin-3-gallate attenuates anesthesia-induced memory deficit in young mice via modulation of nitric oxide expression
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236261/
https://www.ncbi.nlm.nih.gov/pubmed/30320383
http://dx.doi.org/10.3892/mmr.2018.9548
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