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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
- 서은경; 황은숙
- SCOPUS Author ID
- 서은경
; 황은숙
- Issue Date
- 2014
- Journal Title
- Chemistry and Biodiversity
- ISSN
- 1612-1872
- Citation
- Chemistry and Biodiversity vol. 11, no. 12, pp. 1954 - 1962
- Keywords
- Alkaloids; CD4+ T cells; Cell-division rates; IL-2 production; Immunomodulatory activity; Stemona tuberosa; Tuberostemonine alkaloids
- Publisher
- Wiley-VCH Verlag
- Indexed
- SCIE; 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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