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• W2159826428 abstract "Ginsenoside (G) <TEX>$Rp_1$</TEX> is a ginseng saponin derivative with anti-cancer and anti-inflammatory activities. In this study, we examined the mechanism by which G-<TEX>$Rp_1$</TEX> inhibits inflammatory responses of cells. We did this using a strategy in which DNA constructs containing cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) promoters were transfected into HEK293 cells. G-<TEX>$Rp_1$</TEX> strongly inhibited the promoter activities of COX-2 and iNOS; it also inhibited lipopolysaccharide induced upregulation of COX-2 and iNOS mRNA levels in RAW264.7 cells. In HEK293 cells G-<TEX>$Rp_1$</TEX> did not suppress TANK binding kinase 1-, Toll-interleukin-1 receptor-domain-containing adapter-inducing interferon-<TEX>${beta}$</TEX> (TRIF)-, TRIF-related adaptor molecule (TRAM)-, or activation of interferon regulatory factor (IRF)-3 and nuclear factor (NF)-<TEX>${kappa}$</TEX>B by the myeloid differentiation primary response gene (MyD88)-induced. However, G-<TEX>$Rp_1$</TEX> strongly suppressed NF-<TEX>${kappa}$</TEX>B activation induced by I<TEX>${kappa}$</TEX>B kinase (IKK)<TEX>${beta}$</TEX> in HEK293 cells. Consistent with these results, G-<TEX>$Rp_1$</TEX> substantially inhibited IKK<TEX>${beta}$</TEX>-induced phosphorylation of <TEX>$I{kappa}B{alpha}$</TEX> and p65. These results suggest that G-<TEX>$Rp_1$</TEX> is a novel anti-inflammatory ginsenoside analog that can be used to treat IKK<TEX>${beta}$</TEX>/NF-<TEX>${kappa}$</TEX>B-mediated inflammatory diseases." @default.
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• W2159826428 date "2011-06-29" @default.
• W2159826428 modified "2023-09-30" @default.
• W2159826428 title "Ginsenoside Rp₁, a Ginsenoside Derivative, Blocks Promoter Activation of iNOS and COX-2 Genes by Suppression of an IKKβ-mediated NF-κB Pathway in HEK293 Cells" @default.
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• W2159826428 doi "https://doi.org/10.5142/jgr.2011.35.2.200" @default.
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