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Suppression of IL-2 production and proliferation of CD4+ T cells by tuberostemonine O

Title
Suppression of IL-2 production and proliferation of CD4+ T cells by tuberostemonine O
Authors
Jang E.J.Kil Y.-S.Park H.R.Oh S.Kim H.K.Jeong M.G.Seo E.K.Hwang E.S.
Ewha Authors
서은경황은숙
SCOPUS Author ID
서은경scopus; 황은숙scopus
Issue Date
2014
Journal Title
Chemistry and Biodiversity
ISSN
1612-1872JCR Link
Citation
Chemistry and Biodiversity vol. 11, no. 12, pp. 1954 - 1962
Keywords
AlkaloidsCD4+ T cellsCell-division ratesIL-2 productionImmunomodulatory activityStemona tuberosaTuberostemonine alkaloids
Publisher
Wiley-VCH Verlag
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Tuberostemonine stereoisomers are natural alkaloids found in Stemona tuberosa, that are known to have anti-inflammatory and anti-infective properties. Tuberostemonine alkaloids inhibit inflammation by suppressing the expression of inflammatory mediators such as cyclooxygenase and nitric oxide synthase. However, the direct immunomodulatory properties of tuberostemonine alkaloids in T cells have not been elucidated so far. In this study, the activities in T cells of tuberostemonine N (TbN) and a novel alkaloid, tuberostemonine O (TbO), isolated from S. tuberosa, were investigated. Although TbN did not have a significant effect on cytokine production in splenic T cells, TbO selectively suppressed interleukin (IL)-2 production. Moreover, TbO, but not TbN, significantly inhibited IL-2 production by primary CD4+ T cells and delayed the T-cell proliferation in a dose-dependent manner. Addition of excess recombinant IL-2 restored the decreased cell-division rates in TbO-treated CD4+ T cells to control levels. Collectively, these findings suggest that the immunomodulatory effects of TbO occurred by the suppression of IL-2 expression and IL-2-induced T-cell proliferation, suggesting a potential beneficial role of tuberostemonine alkaloids for the control of chronic inflammatory and autoimmune diseases caused by hyperactivated T cells. © 2014 Verlag Helvetica Chimica Acta AG.
DOI
10.1002/cbdv.201400074
Appears in Collections:
약학대학 > 약학과 > Journal papers
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