Ginsenoside Rp1 Exerts Anti-inflammatory Effects via Activation of Dendritic Cells and Regulatory T Cells

被引:19
作者
Bae, Jingyu [1 ]
Koo, Jihye [1 ]
Kim, Soochan [1 ]
Park, Tae-Yoon [2 ]
Kim, Mi-Yeon [1 ]
机构
[1] Soongsil Univ, Dept Bioinformat & Life Sci, Coll Nat Sci, Seoul 156743, South Korea
[2] Yonsei Univ, Dept Biotechnol, Coll Life Sci & Biotechnol, Seoul 120749, South Korea
基金
新加坡国家研究基金会;
关键词
Panax ginseng; Regulatory T cell; Dendritic cell; Ginsenoside Rp1; Inflammation; KAPPA-B PATHWAY; CANCER CELLS; AUTOIMMUNE ENCEPHALOMYELITIS; IN-VIVO; DIFFERENTIATION; SUPPRESSION; ANTIGEN; IL-10; RH-2; MICE;
D O I
10.5142/jgr.2012.36.4.375
中图分类号
Q94 [植物学];
学科分类号
071001 [植物学];
摘要
Ginsenoside Rp1 (G-Rp1) is a saponin derivate that provides anti-metastatic activities through inhibition of the NF-kappa B pathway. In this study, we examined the effects of G-Rp1 on regulatory T cell (Treg) activation. After treatment of splenocytes with G-Rp1, Tregs exhibited upregulation of IL-10 expression, and along with dendritic cells (DCs), these Tregs showed increased cell number compared to other cell populations. The effect of G-Rp1 on Treg number was augmented in the presence of lipopolysaccharide (LPS), which mimics pathological changes that occur during inflammation. However, depletion of DCs prevented the increase in Treg number in the presence of G-Rp1 and/or LPS. In addition, G-Rp1 promoted the differentiation of the memory types of CD4(+)Foxp3(+)CD62L(low) Tregs rather than the generation of new Tregs. In vivo experiments also demonstrated that Tregs and DCs from mice that were fed G-Rp1 for 7 d and then injected with LPS exhibited increased activation compared with those from mice that were injected with LPS alone. Expression of TGF-beta and CTLA4 in Tregs was increased, and upregulation of IL-2 and CD80/CD86 expression by DCs affected the suppressive function of Tregs through IL-2 receptors and CTLA4. These data demonstrate that G-Rp1 exerts anti-inflammatory effects by activating Tregs in vitro and in vivo.
引用
收藏
页码:375 / 382
页数:8
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