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Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis

The death of retinal ganglion cells is a hallmark of many optic neurodegenerative diseases such as glaucoma and retinopathy. Oxidative stress is one of the major reasons to cause the cell death. Oligomeric proanthocyanidin has many health beneficial effects including antioxidative and neuroprotectiv...

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Autores principales: Wang, Hui, Zhang, Chanjuan, Lu, Dan, Shu, Xiaoming, Zhu, Lihong, Qi, Renbing, So, Kwok-Fai, Lu, Daxiang, Xu, Ying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146041/
https://www.ncbi.nlm.nih.gov/pubmed/25206541
http://dx.doi.org/10.3969/j.issn.1673-5374.2013.25.002
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author Wang, Hui
Zhang, Chanjuan
Lu, Dan
Shu, Xiaoming
Zhu, Lihong
Qi, Renbing
So, Kwok-Fai
Lu, Daxiang
Xu, Ying
author_facet Wang, Hui
Zhang, Chanjuan
Lu, Dan
Shu, Xiaoming
Zhu, Lihong
Qi, Renbing
So, Kwok-Fai
Lu, Daxiang
Xu, Ying
author_sort Wang, Hui
collection PubMed
description The death of retinal ganglion cells is a hallmark of many optic neurodegenerative diseases such as glaucoma and retinopathy. Oxidative stress is one of the major reasons to cause the cell death. Oligomeric proanthocyanidin has many health beneficial effects including antioxidative and neuroprotective actions. Here we tested whether oligomeric proanthocyanidin may protect retinal ganglion cells against oxidative stress induced-apoptosis in vitro. Retinal ganglion cells were treated with hydrogen peroxide with or without oligomeric proanthocyanidin. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that treating retinal ganglion cell line RGC-5 cells with 20 μmol/L oligomeric proanthocyanidin significantly decreased the hydrogen peroxide (H(2)O(2)) induced death. Results of flow cytometry and Hoechst staining demonstrated that the death of RGC-5 cells was mainly caused by cell apoptosis. We further found that expression of pro-apoptotic Bax and caspase-3 were significantly decreased while anti-apoptotic Bcl-2 was greatly increased in H(2)O(2) damaged RGC-5 cells with oligomeric proanthocyanidin by western blot assay. Furthermore, in retinal explant culture, the number of surviving retinal ganglion cells in H(2)O(2)-damaged retinal ganglion cells with oligomeric proanthocyanidin was significantly increased. Our studies thus demonstrate that oligomeric proanthocyanidin can protect oxidative stress-injured retinal ganglion cells by inhibiting apoptotic process.
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spelling pubmed-41460412014-09-09 Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis Wang, Hui Zhang, Chanjuan Lu, Dan Shu, Xiaoming Zhu, Lihong Qi, Renbing So, Kwok-Fai Lu, Daxiang Xu, Ying Neural Regen Res Research and Report Article: Traditional Chinese Medicine and Neural Regeneration The death of retinal ganglion cells is a hallmark of many optic neurodegenerative diseases such as glaucoma and retinopathy. Oxidative stress is one of the major reasons to cause the cell death. Oligomeric proanthocyanidin has many health beneficial effects including antioxidative and neuroprotective actions. Here we tested whether oligomeric proanthocyanidin may protect retinal ganglion cells against oxidative stress induced-apoptosis in vitro. Retinal ganglion cells were treated with hydrogen peroxide with or without oligomeric proanthocyanidin. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that treating retinal ganglion cell line RGC-5 cells with 20 μmol/L oligomeric proanthocyanidin significantly decreased the hydrogen peroxide (H(2)O(2)) induced death. Results of flow cytometry and Hoechst staining demonstrated that the death of RGC-5 cells was mainly caused by cell apoptosis. We further found that expression of pro-apoptotic Bax and caspase-3 were significantly decreased while anti-apoptotic Bcl-2 was greatly increased in H(2)O(2) damaged RGC-5 cells with oligomeric proanthocyanidin by western blot assay. Furthermore, in retinal explant culture, the number of surviving retinal ganglion cells in H(2)O(2)-damaged retinal ganglion cells with oligomeric proanthocyanidin was significantly increased. Our studies thus demonstrate that oligomeric proanthocyanidin can protect oxidative stress-injured retinal ganglion cells by inhibiting apoptotic process. Medknow Publications & Media Pvt Ltd 2013-09-05 /pmc/articles/PMC4146041/ /pubmed/25206541 http://dx.doi.org/10.3969/j.issn.1673-5374.2013.25.002 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research and Report Article: Traditional Chinese Medicine and Neural Regeneration
Wang, Hui
Zhang, Chanjuan
Lu, Dan
Shu, Xiaoming
Zhu, Lihong
Qi, Renbing
So, Kwok-Fai
Lu, Daxiang
Xu, Ying
Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis
title Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis
title_full Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis
title_fullStr Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis
title_full_unstemmed Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis
title_short Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis
title_sort oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis
topic Research and Report Article: Traditional Chinese Medicine and Neural Regeneration
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146041/
https://www.ncbi.nlm.nih.gov/pubmed/25206541
http://dx.doi.org/10.3969/j.issn.1673-5374.2013.25.002
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