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Published:
Sep 16, 2014DOI:
10.4314/tjpr.v13i7.9Keywords:
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Main Article Content
Ginsenoside Rb1 Reduces Nitric Oxide Production via Inhibition of Nuclear Factor-κB Activation in Interleukin-1β- Stimulated SW1353 Chondrosarcoma Cells
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
