人参皂苷代谢物K通过抑制T细胞活化发挥抗炎作用

Jingyu Chen, Wei Wei
{"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}
引用次数: 1

摘要

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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信