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Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice

PURPOSE: The purpose of this study was to determine the protective effects of Resveratrol (RESV) on acute bright light-induced retinal degeneration in aged senescence accelerated mouse strain. METHODS: Ten three-month-old male SAMP8 mice (prone to aging) were randomly assigned to two experimental di...

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Autores principales: Liu, Zhirong, Wu, Zhengzheng, Li, Jie, Marmalidou, Anna, Zhang, Ruifan, Yu, Man
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5630371/
https://www.ncbi.nlm.nih.gov/pubmed/29029471
http://dx.doi.org/10.18632/oncotarget.19473
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author Liu, Zhirong
Wu, Zhengzheng
Li, Jie
Marmalidou, Anna
Zhang, Ruifan
Yu, Man
author_facet Liu, Zhirong
Wu, Zhengzheng
Li, Jie
Marmalidou, Anna
Zhang, Ruifan
Yu, Man
author_sort Liu, Zhirong
collection PubMed
description PURPOSE: The purpose of this study was to determine the protective effects of Resveratrol (RESV) on acute bright light-induced retinal degeneration in aged senescence accelerated mouse strain. METHODS: Ten three-month-old male SAMP8 mice (prone to aging) were randomly assigned to two experimental dietary groups: one untreated group and one RESV treatment group (n=20 eyes for each group). After 30 days of treatment, mice were exposed to intense bright light. Ten male SAMR1 mice (resistant to aging) served as control (n=20 eyes). The protective effects of RESV administration on light-induced retinal degeneration in SAMP8 strain as well as the effect of bright light damage in the retinas of SAMP8 mice were analyzed by electroretinography (ERG), retinal histology, mRNA, protein and lipid profile. RESULTS: 68%-85% of a-wave amplitude and 72%-92% of b-wave amplitude were persevered by RESV in SAMP8 mice that were exposed to light damage. Also, RESV preserved their photoreceptor nuclei. mRNA expression of neuroprotective factors leukemia inhibitory factor (LIF), brain derived neurotrophic factor (BDNF), oncostatin M (OSM), cardiotrophin 1(CT-1) and cardiotrophin-like cytokine (CLC) were up-regulated 28, 8, 7, 5 and 9-fold in SAMP8 mice after RESV treatment. In addition, RESV could suppress the NF-κB pathway by down-regulating the expression of pIκB. Light damage led to increase of saturated FA, monoenoic FA, n6 PUFA and n6/n3 ratio and decrease of Docosahexaenoic acid (DHA). There was no significant difference on DHA and the ratio of n6/n3-FA between the untreated and RESV treated SAMP8 mice. CONCLUSIONS: Collectively, our study provides evidence that RESV prevents light-induced retinal damage associated with aging.
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spelling pubmed-56303712017-10-12 Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice Liu, Zhirong Wu, Zhengzheng Li, Jie Marmalidou, Anna Zhang, Ruifan Yu, Man Oncotarget Research Paper PURPOSE: The purpose of this study was to determine the protective effects of Resveratrol (RESV) on acute bright light-induced retinal degeneration in aged senescence accelerated mouse strain. METHODS: Ten three-month-old male SAMP8 mice (prone to aging) were randomly assigned to two experimental dietary groups: one untreated group and one RESV treatment group (n=20 eyes for each group). After 30 days of treatment, mice were exposed to intense bright light. Ten male SAMR1 mice (resistant to aging) served as control (n=20 eyes). The protective effects of RESV administration on light-induced retinal degeneration in SAMP8 strain as well as the effect of bright light damage in the retinas of SAMP8 mice were analyzed by electroretinography (ERG), retinal histology, mRNA, protein and lipid profile. RESULTS: 68%-85% of a-wave amplitude and 72%-92% of b-wave amplitude were persevered by RESV in SAMP8 mice that were exposed to light damage. Also, RESV preserved their photoreceptor nuclei. mRNA expression of neuroprotective factors leukemia inhibitory factor (LIF), brain derived neurotrophic factor (BDNF), oncostatin M (OSM), cardiotrophin 1(CT-1) and cardiotrophin-like cytokine (CLC) were up-regulated 28, 8, 7, 5 and 9-fold in SAMP8 mice after RESV treatment. In addition, RESV could suppress the NF-κB pathway by down-regulating the expression of pIκB. Light damage led to increase of saturated FA, monoenoic FA, n6 PUFA and n6/n3 ratio and decrease of Docosahexaenoic acid (DHA). There was no significant difference on DHA and the ratio of n6/n3-FA between the untreated and RESV treated SAMP8 mice. CONCLUSIONS: Collectively, our study provides evidence that RESV prevents light-induced retinal damage associated with aging. Impact Journals LLC 2017-07-22 /pmc/articles/PMC5630371/ /pubmed/29029471 http://dx.doi.org/10.18632/oncotarget.19473 Text en Copyright: © 2017 Liu et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Liu, Zhirong
Wu, Zhengzheng
Li, Jie
Marmalidou, Anna
Zhang, Ruifan
Yu, Man
Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice
title Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice
title_full Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice
title_fullStr Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice
title_full_unstemmed Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice
title_short Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice
title_sort protective effect of resveratrol against light-induced retinal degeneration in aged samp8 mice
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5630371/
https://www.ncbi.nlm.nih.gov/pubmed/29029471
http://dx.doi.org/10.18632/oncotarget.19473
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