Abstract
Ginseng (Panax ginseng C.A. Mey) is commonly used to treat osteoarthritis (OA) in Chinese traditional medicine (TCM). In this study, we investigated whether ginsenoside retinoblastoma 1 (Rb1), an active component of ginseng, could regulate NO production in chondrocytes and its potential mechanisms of action. SW1353 cells were stimulated with IL-1β in the presence of different concentrations of ginsenoside Rb1. NO concentration was assessed by the Griess reaction. Expression of iNOS, degradation of Iï«Bα and nuclear translocation of NF-κB p65 were determined by Western blot. DNA binding activity of NF-κB complex was evaluated with Trans AM™ kit for p65. We found that ginsenoside Rb1 significantly decreased the NO production and iNOS protein expression in a concentration-dependent manner. Ginsenoside Rb1 markedly decreased the IκBα degradation and nuclear p65 levels, as well as inhibited the DNA binding activity of NF-κB complex. These results suggest that ginsenoside Rb1 inhibits IL-1β-induced NO production through downregulation of NF-κB-dependent iNOS expression in chondrocytes, and reveals potential mechanisms explaining the benefits of ginseng for OA treatment in TCM. Key words: Ginsenoside, retinoblastoma 1 (Rb1), NO, inducible nitric oxide synthase (iNOS), nuclear factor κB (NF-κB), chondrocyte, osteoarthritis.
Highlights
Osteoarthritis (OA) is one of the most common chronic diseases affecting the elderly and is characterized by the abnormal degradation of the cartilage matrix and immoderate deposition of subchondral bone matrix (Li, 2012)
Ginsenoside retinoblastoma 1 (Rb1) inhibited nitric oxide (NO) production in IL-1βinduced SW1353 cells
This effect was abrogated in a dose-dependent manner when SW1353 cells were coincubated with various concentrations of ginsenoside Rb1 (20 to 80 μM), Ginsenoside Rb1 at 40 and 80 μM decreased IL-1β-induced NO production by approximately 24% (p
Summary
Osteoarthritis (OA) is one of the most common chronic diseases affecting the elderly and is characterized by the abnormal degradation of the cartilage matrix and immoderate deposition of subchondral bone matrix (Li, 2012). Osteoarthritic joints exhibit elevated NO production as well as increased amounts of other inflammatory mediators (Charles et al, 1993). NO is generated mainly by inducible nitric oxide synthase (iNOS). Chondrocytes, the cellular occupants of cartilage and central to maintaining the integrity of the matrix, are the main cellular source of NO and iNOS generation in OA (Grabowski et al, 1997). NO is considered as a pro-inflammation agent as well as a potent catabolic mediator in OA since it promotes the production of inflammatory cytokines (Wang et al, 1997), activates matrix metalloproteinases (Murrell et al, 1995) and inhibits the synthesis of collagen and proteoglycan (Cao et al, 1997)
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