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Anti-apoptotic Activity of Ginsenoside Rb(1) in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3

Chondrocyte apoptosis has been recognized as an important factor in the pathogenesis of osteoarthritis (OA). Hydrogen peroxide (H(2)O(2)), which produces reactive oxygen species, reportedly induces apoptosis in chondrocytes. The ginsenoside Rb(1) (GRb(1)) is the principal component in ginseng and ha...

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Autores principales: Na, Ji-Young, Kim, Sokho, Song, Kibbeum, Lim, Kyu-Hee, Shin, Gee-Wook, Kim, Jong-Hoon, Kim, Bumseok, Kwon, Young-Bae, Kwon, Jungkee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Ginseng 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659597/
https://www.ncbi.nlm.nih.gov/pubmed/23717124
http://dx.doi.org/10.5142/jgr.2012.36.3.242
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author Na, Ji-Young
Kim, Sokho
Song, Kibbeum
Lim, Kyu-Hee
Shin, Gee-Wook
Kim, Jong-Hoon
Kim, Bumseok
Kwon, Young-Bae
Kwon, Jungkee
author_facet Na, Ji-Young
Kim, Sokho
Song, Kibbeum
Lim, Kyu-Hee
Shin, Gee-Wook
Kim, Jong-Hoon
Kim, Bumseok
Kwon, Young-Bae
Kwon, Jungkee
author_sort Na, Ji-Young
collection PubMed
description Chondrocyte apoptosis has been recognized as an important factor in the pathogenesis of osteoarthritis (OA). Hydrogen peroxide (H(2)O(2)), which produces reactive oxygen species, reportedly induces apoptosis in chondrocytes. The ginsenoside Rb(1) (GRb(1)) is the principal component in ginseng and has been shown to have a variety of biological activities, such as anti-arthritis, anti-inflammation, and anti-tumor activities. In this study, we evaluated the effects of G-Rb(1) on the mitochondrial permeability transition (MPT) and caspase-3 activity of chondrocyte apoptosis induced by H(2)O(2). Cultured rat articular chondrocytes were exposed to H(2)O(2) with or without G-Rb(1) and assessed for viability, MPT, Bcl-xL/Bax expression, caspase-3 activity, and apoptosis. The co-treatment with G-Rb(1) showed an inhibition of MPT, caspase-3 activity, and cell death. Additionally, the levels of the apoptotic protein Bax were significantly lower and the levels of the anti-apoptotic protein Bcl-xL were higher compared with H(2)O(2) treatment alone. The results of this study demonstrate that G-Rb(1) protects chondrocytes against H(2)O(2)-induced apoptosis, at least in part via the inhibition of MPT and caspase-3 activity. These results demonstrate that G-Rb(1) is a potentially useful drug for the treatment of OA patients.
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spelling pubmed-36595972013-05-28 Anti-apoptotic Activity of Ginsenoside Rb(1) in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3 Na, Ji-Young Kim, Sokho Song, Kibbeum Lim, Kyu-Hee Shin, Gee-Wook Kim, Jong-Hoon Kim, Bumseok Kwon, Young-Bae Kwon, Jungkee J Ginseng Res Articles Chondrocyte apoptosis has been recognized as an important factor in the pathogenesis of osteoarthritis (OA). Hydrogen peroxide (H(2)O(2)), which produces reactive oxygen species, reportedly induces apoptosis in chondrocytes. The ginsenoside Rb(1) (GRb(1)) is the principal component in ginseng and has been shown to have a variety of biological activities, such as anti-arthritis, anti-inflammation, and anti-tumor activities. In this study, we evaluated the effects of G-Rb(1) on the mitochondrial permeability transition (MPT) and caspase-3 activity of chondrocyte apoptosis induced by H(2)O(2). Cultured rat articular chondrocytes were exposed to H(2)O(2) with or without G-Rb(1) and assessed for viability, MPT, Bcl-xL/Bax expression, caspase-3 activity, and apoptosis. The co-treatment with G-Rb(1) showed an inhibition of MPT, caspase-3 activity, and cell death. Additionally, the levels of the apoptotic protein Bax were significantly lower and the levels of the anti-apoptotic protein Bcl-xL were higher compared with H(2)O(2) treatment alone. The results of this study demonstrate that G-Rb(1) protects chondrocytes against H(2)O(2)-induced apoptosis, at least in part via the inhibition of MPT and caspase-3 activity. These results demonstrate that G-Rb(1) is a potentially useful drug for the treatment of OA patients. The Korean Society of Ginseng 2012-07 /pmc/articles/PMC3659597/ /pubmed/23717124 http://dx.doi.org/10.5142/jgr.2012.36.3.242 Text en Copyright ©2012, The Korean Society of Ginseng http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Articles
Na, Ji-Young
Kim, Sokho
Song, Kibbeum
Lim, Kyu-Hee
Shin, Gee-Wook
Kim, Jong-Hoon
Kim, Bumseok
Kwon, Young-Bae
Kwon, Jungkee
Anti-apoptotic Activity of Ginsenoside Rb(1) in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3
title Anti-apoptotic Activity of Ginsenoside Rb(1) in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3
title_full Anti-apoptotic Activity of Ginsenoside Rb(1) in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3
title_fullStr Anti-apoptotic Activity of Ginsenoside Rb(1) in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3
title_full_unstemmed Anti-apoptotic Activity of Ginsenoside Rb(1) in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3
title_short Anti-apoptotic Activity of Ginsenoside Rb(1) in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3
title_sort anti-apoptotic activity of ginsenoside rb(1) in hydrogen peroxide-treated chondrocytes: stabilization of mitochondria and the inhibition of caspase-3
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659597/
https://www.ncbi.nlm.nih.gov/pubmed/23717124
http://dx.doi.org/10.5142/jgr.2012.36.3.242
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