Abstract
Purpose: To investigate the effect and the potential mechanisms of ginsenoside Rb1 on nitric oxide (NO) production in chondrocytes.Methods: SW1353 chondrosarcoma cells were stimulated with interleukin-1β (IL-1β) in the presence of 20, 40, 80 μM ginsenoside Rb1. NO concentration was assessed by the Griess reaction. Expression of inducible nitric oxide synthase (iNOS), content of inhibitor of NF-κB (IκB)α and nuclear level of nuclear factor (NF)-κB p65 were determined by Western blot. DNA binding activity of NF-κB was evaluated with Trans AM™ kit for NF-κB p65.Results: Ginsenoside Rb1 (40 and 80 μM) significantly decreased NO level by 24 (p < 0.05) and 46 % (p < 0.01), as well as iNOS protein expression by 40 and 55 % (p < 0.01), respectively, in IL-1β- stimulated SW1353 cells. Ginsenoside Rb1 (40 and 80 μM) also markedly elevated IκBα protein content by 200 and 260 % (p < 0.01), reduced the nuclear level of p65 protein by 30 and 40 % (p < 0.01), as well as decreased the DNA binding activity of NF-κB by 40 and 50 % (both p < 0.01), respectively, in IL- 1β-stimulated SW1353 cells.Conclusion: These results suggest that ginsenoside Rb1 inhibits IL-1β-induced NO production through downregulation of NF-κB-dependent iNOS expression in chondrocytes, and also underlines the potential mechanisms of ginseng activity in OA treatment of TCM. Keywords: Ginsenoside Rb1, Nitric oxide, Nuclear factor-κB, Chondrocytes, 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
Ginsenoside Rb1 at 20 μM did not show any effect on IL-1β-induced nitric oxide (NO) production in SW1353 cells (Fig 1A)
Because the translocation of nuclear factor (NF)-κB to the nucleus depends on degradation of IκBα, we investigated whether ginsenoside Rb1 could affect this process
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. A growing body of evidence supports the fact that nitric oxide (NO) plays a role in the pathological development of OA [1]. NO production as well as increased amounts of other inflammatory mediators [2]. OA patients exhibited markers of enhanced NO production in their urine, serum, and synovial fluid [3]. NO is generated principally by inducible NO 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 [4].
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