{"title":"人参皂苷代谢物K通过抑制T细胞活化发挥抗炎作用","authors":"Jingyu Chen, Wei Wei","doi":"10.14800/ICS.725","DOIUrl":null,"url":null,"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.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2015-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Ginsenoside metabolite compound K exerts anti-inflammatory effect via suppressing T cell activation\",\"authors\":\"Jingyu Chen, Wei Wei\",\"doi\":\"10.14800/ICS.725\",\"DOIUrl\":null,\"url\":null,\"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.\",\"PeriodicalId\":13679,\"journal\":{\"name\":\"Inflammation and cell signaling\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2015-03-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Inflammation and cell signaling\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.14800/ICS.725\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Inflammation and cell signaling","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14800/ICS.725","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Ginsenoside metabolite compound K exerts anti-inflammatory effect via suppressing T cell activation
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.