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Rhizoma Paridis total saponins alleviate H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway
Rhizoma Paridis total saponins (RPTS) is an active substance isolated from the traditional Chinese medicine Rhizoma Paridis, which possesses multiple biological activities. The aim of the present study was to explore the roles and mechanisms of RPTS in oxidative stress injury of ARPE-19 human retina...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6896395/ https://www.ncbi.nlm.nih.gov/pubmed/31746361 http://dx.doi.org/10.3892/mmr.2019.10827 |
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author | Zhao, Baocheng Wang, Zhenjun Han, Jiagang Wei, Guanghui Yi, Bingqiang Li, Zhulin |
author_facet | Zhao, Baocheng Wang, Zhenjun Han, Jiagang Wei, Guanghui Yi, Bingqiang Li, Zhulin |
author_sort | Zhao, Baocheng |
collection | PubMed |
description | Rhizoma Paridis total saponins (RPTS) is an active substance isolated from the traditional Chinese medicine Rhizoma Paridis, which possesses multiple biological activities. The aim of the present study was to explore the roles and mechanisms of RPTS in oxidative stress injury of ARPE-19 human retinal pigment epithelial cells. Cell viability, reactive oxygen species (ROS) levels, mitochondrial membrane potential (MMP) and apoptosis were determined by Cell Counting kit-8 assay and flow cytometry, respectively. Enzyme-linked immunosorbent assay was performed to detect the expression of oxidative stress markers. Western blotting and reverse transcription-quantitative polymerase chain reaction were used to determine the expression levels of related genes and proteins. The results revealed that RPTS enhanced cell viability and reduced H(2)O(2)-induced oxidative stress of ARPE-19 human retinal pigment epithelial cells. RPTS increased the MMP of ARPE-19 cells compared with in H(2)O(2)-treated ARPE-19 cells. In addition, RPTS suppressed ROS production and apoptosis of H(2)O(2)-treated ARPE-19 cells. Additionally, RPTS modulated the expression levels of apoptosis-associated proteins and the nuclear factor 2-related factor 2 (Nrf2) pathway. In conclusion, RPTS alleviated H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway. The potential effects of RPTS on protection against H(2)O(2)-induced apoptosis of ARPE-19 cells suggested that RPTS may be a potential therapeutic target for preventing age-related macular degeneration. |
format | Online Article Text |
id | pubmed-6896395 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-68963952019-12-09 Rhizoma Paridis total saponins alleviate H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway Zhao, Baocheng Wang, Zhenjun Han, Jiagang Wei, Guanghui Yi, Bingqiang Li, Zhulin Mol Med Rep Articles Rhizoma Paridis total saponins (RPTS) is an active substance isolated from the traditional Chinese medicine Rhizoma Paridis, which possesses multiple biological activities. The aim of the present study was to explore the roles and mechanisms of RPTS in oxidative stress injury of ARPE-19 human retinal pigment epithelial cells. Cell viability, reactive oxygen species (ROS) levels, mitochondrial membrane potential (MMP) and apoptosis were determined by Cell Counting kit-8 assay and flow cytometry, respectively. Enzyme-linked immunosorbent assay was performed to detect the expression of oxidative stress markers. Western blotting and reverse transcription-quantitative polymerase chain reaction were used to determine the expression levels of related genes and proteins. The results revealed that RPTS enhanced cell viability and reduced H(2)O(2)-induced oxidative stress of ARPE-19 human retinal pigment epithelial cells. RPTS increased the MMP of ARPE-19 cells compared with in H(2)O(2)-treated ARPE-19 cells. In addition, RPTS suppressed ROS production and apoptosis of H(2)O(2)-treated ARPE-19 cells. Additionally, RPTS modulated the expression levels of apoptosis-associated proteins and the nuclear factor 2-related factor 2 (Nrf2) pathway. In conclusion, RPTS alleviated H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway. The potential effects of RPTS on protection against H(2)O(2)-induced apoptosis of ARPE-19 cells suggested that RPTS may be a potential therapeutic target for preventing age-related macular degeneration. D.A. Spandidos 2020-01 2019-11-20 /pmc/articles/PMC6896395/ /pubmed/31746361 http://dx.doi.org/10.3892/mmr.2019.10827 Text en Copyright: © Zhao 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 Zhao, Baocheng Wang, Zhenjun Han, Jiagang Wei, Guanghui Yi, Bingqiang Li, Zhulin Rhizoma Paridis total saponins alleviate H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway |
title | Rhizoma Paridis total saponins alleviate H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway |
title_full | Rhizoma Paridis total saponins alleviate H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway |
title_fullStr | Rhizoma Paridis total saponins alleviate H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway |
title_full_unstemmed | Rhizoma Paridis total saponins alleviate H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway |
title_short | Rhizoma Paridis total saponins alleviate H(2)O(2)-induced oxidative stress injury by upregulating the Nrf2 pathway |
title_sort | rhizoma paridis total saponins alleviate h(2)o(2)-induced oxidative stress injury by upregulating the nrf2 pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6896395/ https://www.ncbi.nlm.nih.gov/pubmed/31746361 http://dx.doi.org/10.3892/mmr.2019.10827 |
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