Induction of TGF-β and IL-10 production in dendritic cells using astilbin to inhibit dextran sulfate sodium-induced colitis

被引:26
作者
Ding, Yanbing [1 ]
Liang, Yu [1 ]
Deng, Bin [1 ]
Qiao, Ahui [1 ]
Wu, Keyan [1 ]
Xiao, Weiming [1 ]
Gong, Weijuan [2 ]
机构
[1] Yangzhou Univ, Clin Coll 2, Dept Gastroenterol, Yangzhou 225001, Jiangsu, Peoples R China
[2] Yangzhou Univ, Sch Med, Dept Immunol, Yangzhou 225001, Jiangsu, Peoples R China
关键词
Astilbin; Dendritic cells; Colitis; INFLAMMATORY-BOWEL-DISEASE; COLLAGEN-INDUCED ARTHRITIS; PATHOGENESIS; HYPERSENSITIVITY; THERAPY; LEAVES;
D O I
10.1016/j.bbrc.2014.02.136
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Astilbin, a major bioactive compound from Rhizome smilacis glabrae, has been reported to possess anti-inflammatory properties. Our study first evaluated astilbin on dextran sulfate sodium (DSS)-induced acute colitis in mice. By intraperitoneal injection of astilbin, the severity of colitis was attenuated, and the serum levels of IL-10 and TGF-beta were increased. Using flow cytometry, a higher number of IL-10(+) dendritic cells (DCs) and TGF-beta(+) DCs and a lower number of CD86(+) DCs, IL-12 p40(+) DCs, and IL-10(+) DCs were detected in the spleen of mice with colitis after astilbin treatment. The administration of astilbin also resulted in the upregulation of CD103(+) expression in colonic DCs. In a coculture system, murine bone marrow-derived DCs pretreated with astilbin resulted in an enhanced production of CD4(+)CD25(+)Foxp3(+) T cells. The results of this study show that astilbin could be a candidate drug for inflammatory bowel disease by mediating the regulatory functions of DCs. (C) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:529 / 534
页数:6
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