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Echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina
OBJECTIVE: To investigate whether echinacoside (ECH) protects the retina against ischemia/reperfusion (I/R) injury and the underlying mechanisms. METHODS: Adult male Wistar rats were randomly divided into four groups: sham, sham plus ECH, I/R plus vehicle, and I/R plus ECH. Before the retinal I/R in...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Molecular Vision
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6279312/ https://www.ncbi.nlm.nih.gov/pubmed/30581281 |
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author | Li, Lin Wang, YeFei Qin, XiuHong Zhang, Jing Zhang, ZhenZhen |
author_facet | Li, Lin Wang, YeFei Qin, XiuHong Zhang, Jing Zhang, ZhenZhen |
author_sort | Li, Lin |
collection | PubMed |
description | OBJECTIVE: To investigate whether echinacoside (ECH) protects the retina against ischemia/reperfusion (I/R) injury and the underlying mechanisms. METHODS: Adult male Wistar rats were randomly divided into four groups: sham, sham plus ECH, I/R plus vehicle, and I/R plus ECH. Before the retinal I/R injury produced by high intraocular pressure (HOP), ECH was administered (20 mg/kg daily) for 7 days. The level of retinal cell damage was evaluated using Fluoro-Gold (FG) retrograde labeling and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) analysis 7 days after I/R. Optic nerve histology was analyzed with transmission electron microscopy. Levels of retinal malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were determined. The expression of apoptosis-associated factors (Apaf-1, Parp, and Bad) were analyzed with western blotting and quantitative real-time PCR (qPCR). The production of proinflammatory cytokines (tumor necrosis factor-α [TNFα], interleukin-1 beta [IL-1β], and IL-6) was analyzed with enzyme-linked immunosorbent assay (ELISA) 7 days after the I/R injury as well. RESULTS: The administration of ECH not only preserved retinal morphology but also attenuated retinal inflammation and apoptosis at 7 days after the I/R injury and decreased I/R-induced oxidative stress in the retina statistically significantly. CONCLUSIONS: ECH protected against I/R-induced retinal injury, via activation of antioxidant enzymes and suppression of inflammation. Therefore, ECH could be a potential therapeutic candidate for the treatment and management of I/R retinal diseases. |
format | Online Article Text |
id | pubmed-6279312 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Molecular Vision |
record_format | MEDLINE/PubMed |
spelling | pubmed-62793122018-12-21 Echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina Li, Lin Wang, YeFei Qin, XiuHong Zhang, Jing Zhang, ZhenZhen Mol Vis Research Article OBJECTIVE: To investigate whether echinacoside (ECH) protects the retina against ischemia/reperfusion (I/R) injury and the underlying mechanisms. METHODS: Adult male Wistar rats were randomly divided into four groups: sham, sham plus ECH, I/R plus vehicle, and I/R plus ECH. Before the retinal I/R injury produced by high intraocular pressure (HOP), ECH was administered (20 mg/kg daily) for 7 days. The level of retinal cell damage was evaluated using Fluoro-Gold (FG) retrograde labeling and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) analysis 7 days after I/R. Optic nerve histology was analyzed with transmission electron microscopy. Levels of retinal malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were determined. The expression of apoptosis-associated factors (Apaf-1, Parp, and Bad) were analyzed with western blotting and quantitative real-time PCR (qPCR). The production of proinflammatory cytokines (tumor necrosis factor-α [TNFα], interleukin-1 beta [IL-1β], and IL-6) was analyzed with enzyme-linked immunosorbent assay (ELISA) 7 days after the I/R injury as well. RESULTS: The administration of ECH not only preserved retinal morphology but also attenuated retinal inflammation and apoptosis at 7 days after the I/R injury and decreased I/R-induced oxidative stress in the retina statistically significantly. CONCLUSIONS: ECH protected against I/R-induced retinal injury, via activation of antioxidant enzymes and suppression of inflammation. Therefore, ECH could be a potential therapeutic candidate for the treatment and management of I/R retinal diseases. Molecular Vision 2018-11-25 /pmc/articles/PMC6279312/ /pubmed/30581281 Text en Copyright © 2018 Molecular Vision. http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited, used for non-commercial purposes, and is not altered or transformed. |
spellingShingle | Research Article Li, Lin Wang, YeFei Qin, XiuHong Zhang, Jing Zhang, ZhenZhen Echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina |
title | Echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina |
title_full | Echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina |
title_fullStr | Echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina |
title_full_unstemmed | Echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina |
title_short | Echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina |
title_sort | echinacoside protects retinal ganglion cells from ischemia/reperfusion-induced injury in the rat retina |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6279312/ https://www.ncbi.nlm.nih.gov/pubmed/30581281 |
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