Abstract
Ginsenoside metabolite compound K (CK, 20-O-D-glucopyranosyl-20(S)-protopanaxadiol), a novel ginsenoside metabolite, belongs to dammarane-type triterpene saponins according to its structure. The anti-inflammatory activity of CK has been identified in several studies. Our previous study demonstrated that CK exerted anti-inflammatory effect on collagen-induced arthritis (CIA) and adjuvant-induced arthritis (AA) animal models, and this effect was due to inhibiting the abnormal activation and differentiation of T cells. Our recent study showed that the inhibitory effect of CK on T cell activation was related to suppressing CCL21-CCR7-mediated migration of dendritic cells (DCs) and signals between T cells and DCs. In this brief review, we summarize recent studies on the anti-inflammatory effect of CK and highlight recent advances in our understanding of how CK contributes to the anti-inflammatory effect via suppressing T cell activation in autoimmune conditions. Elucidating the potential mechanism by which CK contributes to the anti-inflammatory effect may provide a rationale for development of CK as new therapeutic agents in treatment of inflammatory and autoimmune disease.
Highlights
Ginsenoside metabolite compound K (CK, C36H62O8) is a kind of dammarane-type triterpene saponins
Our recent study showed that the inhibitory effect of CK on T cell activation was due to suppressing CCL21-CCR7-mediated migration of dendritic cells (DCs) and signals between T cells and DCs
CK markedly inhibited the production of the pro-inflammatory cytokines and suppressed the activation of interleukin-1 receptor-associated kinase-1 (IRAK-1), inhibitor κB kinase β (IKKβ), nuclear factor κB (NF-κB), and mitogen-activated protein kinases (MAPKs) (ERK, JNK, and p-38) [4]
Summary
Ginsenoside metabolite compound K (CK, C36H62O8) is a kind of dammarane-type triterpene saponins. Our previous studies showed that CK alleviated adjuvant-induced arthritis (AA) and collagen-induced arthritis (CIA) via suppressing T cell activation. Elucidating the possible mechanism of CK responsible for the anti-inflammatory effect may provide a rationale for development of CK as new therapeutic agents in treatment of inflammatory and autoimmune disease.
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