Ginsenoside metabolite compound K exerts anti-inflammatory effect via suppressing T cell activation

Jingyu Chen, Wei Wei
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引用次数: 1

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.
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人参皂苷代谢物K通过抑制T细胞活化发挥抗炎作用
人参皂苷代谢物化合物K (CK, 20-O-D-glucopyranosyl-20(S)-protopanaxadiol)是一种新型人参皂苷代谢物,根据其结构属于达马烷型三萜皂苷。CK的抗炎活性已在多项研究中得到证实。我们前期研究表明,CK对胶原诱导关节炎(CIA)和佐剂诱导关节炎(AA)动物模型具有抗炎作用,其作用机制是抑制T细胞的异常活化和分化。我们最近的研究表明,CK对T细胞活化的抑制作用与抑制ccl21 - ccr7介导的树突状细胞(dc)的迁移和T细胞与dc之间的信号有关。在这篇简短的综述中,我们总结了最近关于CK抗炎作用的研究,并重点介绍了在自身免疫性疾病中CK如何通过抑制T细胞激活来促进抗炎作用的最新进展。阐明CK参与抗炎作用的潜在机制可能为开发CK作为治疗炎症和自身免疫性疾病的新药物提供理论依据。
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