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KMID : 0861020100250020129
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Korea Journal of Herbology
2010 Volume.25 No. 2 p.129 ~ p.136
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Effect of Sinapis alba L. on expression of interferon-gamma and interleukin-4 production in anti-CD3/anti-CD28-stimulated CD4(+) T cells
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Park Dae-Jung
Lee Jang-Cheon
Lee Young-Cheol
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Abstract
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Objective：Sinapis alba L. (SA) is a korean traditional herbal medicine that is usually used to prevent or treat inflammatory diseases, such as respiratory infection and rheumatoid arthritis. However, the effects of SA supplementation in vitro on serum antibody levels, splenocyte and peritoneal macrophage immune responses have not yet been determined. In this study, we examined the effect of SA on the production of Th1/Th2 cytokines.
Methods：Splenocytes were isolated from naive C57BL/6 mice. Cells were enriched for CD4+ cell populations by first staining the cells with anti-CD4 (BD PharMingen, Calif, USA). CD4+ T cells were selected on a (CS) column, and the flow-through was collected as CD4+ T cells. Isolated cells were activated by overnight incubation on 24-well plates coated with 1μg/mL anti-CD3, 1μg/mL anti-CD28 and with SA (100μg/mL). Primary macrophages were collected from the peritoneal cavities of mice (8-week-old female C57BL/6). The peritoneal macrophages were washed and plated with RPMI-1640 overnight for the experiments. After 48-hours cultures, samples were centrifuged at 2000 rpm for 10 minutes, and the supernatants were stored at ?80℃. Mouse IL-4, IFN-γ and TNF-α were quantified using ELISA kits (BioSource International, Camarillo, Calif, USA) according to the manufacturer’s protocols.
Results：SA at 100ug/ml decreased the generation of Th1 cytokine (IFN-γ) by 0.5-fold. However, SA has no effect on Th2 (IL-4) production.
Conclusions：These results suggest that SA may play an important role in the control of T-cell-mediated autoimmunity by down-regulation of Th1 cytokine (especially IFN-γ, TNF-α). These data may contribute to the design of new immunomodulating treatments for a group of autoimmune diseases.
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KEYWORD
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Sinapis alba L. (SA), IFN-γ, TNF-α, Th1, Th2
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