Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
Vol. 13, No. 7, 2014, pp. 1071-1078
Bioline Code: pr14149
Full paper language: English
Document type: Research Article
Document available free of charge
Tropical Journal of Pharmaceutical Research, Vol. 13, No. 7, 2014, pp. 1071-1078
© Copyright 2014 - Tropical Journal of Pharmaceutical Research
Ginsenoside Rb1 Reduces Nitric Oxide Production via Inhibition of Nuclear Factor-κB Activation in Interleukin-1β- Stimulated SW1353 Chondrosarcoma Cells|
Jia, Ping; Chen, Gang; Li, Rongheng; Rong, Xiaofeng; Zhou, Guoqing & Zhong, Yu
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 AMTM 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.
Ginsenoside Rb1; Nitric oxide; Nuclear factor-κB; Chondrocytes; Osteoarthritis
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