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...
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 ${\mu}M$ ginsenoside $Rb_1$ and/or 500 ${\mu}M$ hydrogen peroxide ($H_2O_2$) 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 $H_2O_2$-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 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 ${\mu}M$ ginsenoside $Rb_1$ and/or 500 ${\mu}M$ hydrogen peroxide ($H_2O_2$) 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 $H_2O_2$-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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제안 방법
Therefore, using antioxidants to protect against free radicals may be important the regulation of OA. In this study, H2O2 was employed to create an oxidative stress environment, and the effect of ginsenoside Rb1 on the regulation of various genes in H2O2-stimulated chondrocytes was evaluated. A previous study demonstrated the anti-oxidative and anti-inflammatory effects of ginsenoside Rb1 on 6-hydroxydopamine-treated human dopaminergic cells [21] and lipopolysaccharidetreated RAW 264.
Despite several studies in the literature detailing the antioxidant effects of ginsenoside Rb1, the mechanisms underlying protective effects at the chondrocyte cellular level have not been reported. In this study, we evaluated the protective effects of ginsenoside Rb1 on rat articular chondrocytes and the molecular mechanisms involved in the protection.
대상 데이터
Polymerase chain reaction was carried out in 48-well plates using the ABI Step One Plus Sequence Detection System (Applied Biosystems). All experiments were performed in triplicate.
All experiments were performed when cells reached confluence within the fi rst passage. Ginsenoside Rb1 was purchased from Ambo Institute (Daejeon, Korea).
성능/효과
By detecting major proteins and infl ammatory genes related to chondrogenic enzymes, we determined that ginsenoside Rb1 plays a protective role in articular chondrocytes. In conclusion, the present study demonstrated the protective effect of ginsenoside Rb1 on chondrocytes and provided new insight into the medicinal qualities of ginseng extracts. Our results suggest the possibility of including ginsenoside Rb1 in therapeutic interventions for OA.
Among members of the MMP superfamily, MMP1 and MMP13 have been shown to degrade type II collagen in OA. Our results revealed that ginsenoside Rb1 antagonized chondrogenic infl ammatory genes (MMP1 and MMP13) and agonized chondrogenic genes (type II collagen and SOX8) to protect against H2O2-induced oxidative stress (Fig. 5). These results suggest that ginsenoside Rb1 has potential for use as a therapeutic agent for OA due to this compound’s anti-infl ammatory effects.
NO is generated by activated iNOS during inflammatory processes [23]. Our results showed that H2O2-elicited NO, iNOS, and ROS production were significantly suppressed by ginsenoside Rb1 (Figs. 3 and 4). NO can induce intracellular signal transduction and inflammatory gene activation.
Real-time reverse transcription polymerase chain reaction analysis for chondrogenic genes (collagen type II and SOX9) and chondrogenic infl ammatory genes (MMP1 and MMP13) was performed as described in Materials and Methods section. Results revealed that ginsenoside Rb1 increased chondrogenic gene expression and reduced chondrogenic infl ammatory gene expression. Values are expressed as mean±SEM of three independent experiments, *p<0.
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