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Protective Effect of Ginsenoside Rb(1) on Hydrogen Peroxide-induced Oxidative Stress in Rat Articular Chondrocytes

The abnormal maturation and ossification of articular chondrocytes play a central role in the pathogenesis of osteoarthritis (OA). Inhibiting the enzymatic degradation of the extracellular matrix and maintaining the cellular phenotype are two of the major goals of interest in managing OA. Ginseng is...

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Autores principales: Kim, Sokho, Na, Ji-Young, Song, Ki-Bbeum, Choi, Dea-Seung, Kim, Jong-Hoon, 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/PMC3659580/
https://www.ncbi.nlm.nih.gov/pubmed/23717116
http://dx.doi.org/10.5142/jgr.2012.36.2.161
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author Kim, Sokho
Na, Ji-Young
Song, Ki-Bbeum
Choi, Dea-Seung
Kim, Jong-Hoon
Kwon, Young-Bae
Kwon, Jungkee
author_facet Kim, Sokho
Na, Ji-Young
Song, Ki-Bbeum
Choi, Dea-Seung
Kim, Jong-Hoon
Kwon, Young-Bae
Kwon, Jungkee
author_sort Kim, Sokho
collection PubMed
description The abnormal maturation and ossification of articular chondrocytes play a central role in the pathogenesis of osteoarthritis (OA). Inhibiting the enzymatic degradation of the extracellular matrix and maintaining the cellular phenotype are two of the major goals of interest in managing OA. Ginseng is frequently taken orally, as a crude substance, as a traditional medicine in Asian countries. Ginsenoside Rb(1), a major component of ginseng that contains an aglycone with a dammarane skeleton, has been reported to exhibit various biological activities, including anti-inflammatory and anti-tumor effects. However, a chondroprotective effect of ginsenoside Rb(1) related to OA has not yet been reported. The purpose of this study was to demonstrate the chondroprotective effect of ginsenoside Rb(1) on the regulation of pro-inflammatory factors and chondrogenic genes. Cultured rat articular chondrocytes were treated with 100 μM ginsenoside Rb(1) and/or 500 μM hydrogen peroxide (H(2)O(2)) and assessed for viability, reactive oxygen species production, nitric oxide (NO) release, and chondrogenic gene expression. Ginsenoside Rb(1) treatment resulted in reductions in the levels of pro-inflammatory cytokine and NO in H(2)O(2)-treated chondrocytes. The expression levels of chondrogenic genes, such as type II collagen and SOX9, were increased in the presence of ginsenoside Rb(1), whereas the expression levels of inflammatory genes related to chondrocytes, such as MMP1 and MMP13, were reduced by approximately 50%. These results suggest that ginsenoside Rb(1) has potential for use as a therapeutic agent in OA patients.
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spelling pubmed-36595802013-05-28 Protective Effect of Ginsenoside Rb(1) on Hydrogen Peroxide-induced Oxidative Stress in Rat Articular Chondrocytes Kim, Sokho Na, Ji-Young Song, Ki-Bbeum Choi, Dea-Seung Kim, Jong-Hoon Kwon, Young-Bae Kwon, Jungkee J Ginseng Res Articles The abnormal maturation and ossification of articular chondrocytes play a central role in the pathogenesis of osteoarthritis (OA). Inhibiting the enzymatic degradation of the extracellular matrix and maintaining the cellular phenotype are two of the major goals of interest in managing OA. Ginseng is frequently taken orally, as a crude substance, as a traditional medicine in Asian countries. Ginsenoside Rb(1), a major component of ginseng that contains an aglycone with a dammarane skeleton, has been reported to exhibit various biological activities, including anti-inflammatory and anti-tumor effects. However, a chondroprotective effect of ginsenoside Rb(1) related to OA has not yet been reported. The purpose of this study was to demonstrate the chondroprotective effect of ginsenoside Rb(1) on the regulation of pro-inflammatory factors and chondrogenic genes. Cultured rat articular chondrocytes were treated with 100 μM ginsenoside Rb(1) and/or 500 μM hydrogen peroxide (H(2)O(2)) and assessed for viability, reactive oxygen species production, nitric oxide (NO) release, and chondrogenic gene expression. Ginsenoside Rb(1) treatment resulted in reductions in the levels of pro-inflammatory cytokine and NO in H(2)O(2)-treated chondrocytes. The expression levels of chondrogenic genes, such as type II collagen and SOX9, were increased in the presence of ginsenoside Rb(1), whereas the expression levels of inflammatory genes related to chondrocytes, such as MMP1 and MMP13, were reduced by approximately 50%. These results suggest that ginsenoside Rb(1) has potential for use as a therapeutic agent in OA patients. The Korean Society of Ginseng 2012-04 /pmc/articles/PMC3659580/ /pubmed/23717116 http://dx.doi.org/10.5142/jgr.2012.36.2.161 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
Kim, Sokho
Na, Ji-Young
Song, Ki-Bbeum
Choi, Dea-Seung
Kim, Jong-Hoon
Kwon, Young-Bae
Kwon, Jungkee
Protective Effect of Ginsenoside Rb(1) on Hydrogen Peroxide-induced Oxidative Stress in Rat Articular Chondrocytes
title Protective Effect of Ginsenoside Rb(1) on Hydrogen Peroxide-induced Oxidative Stress in Rat Articular Chondrocytes
title_full Protective Effect of Ginsenoside Rb(1) on Hydrogen Peroxide-induced Oxidative Stress in Rat Articular Chondrocytes
title_fullStr Protective Effect of Ginsenoside Rb(1) on Hydrogen Peroxide-induced Oxidative Stress in Rat Articular Chondrocytes
title_full_unstemmed Protective Effect of Ginsenoside Rb(1) on Hydrogen Peroxide-induced Oxidative Stress in Rat Articular Chondrocytes
title_short Protective Effect of Ginsenoside Rb(1) on Hydrogen Peroxide-induced Oxidative Stress in Rat Articular Chondrocytes
title_sort protective effect of ginsenoside rb(1) on hydrogen peroxide-induced oxidative stress in rat articular chondrocytes
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659580/
https://www.ncbi.nlm.nih.gov/pubmed/23717116
http://dx.doi.org/10.5142/jgr.2012.36.2.161
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