Suppressive Effects of T-412, a Flavone on Interleukin-4 Production in T Cells
- Authors
- Jin, Mirim; Park, Sunyoung; Pyo, Myoung Yun
- Issue Date
- Nov-2009
- Publisher
- PHARMACEUTICAL SOC JAPAN
- Keywords
- 7,8,4 '-trihydroxyflavone; flavone; interleukin-4; T cell; anti-allergic agent
- Citation
- BIOLOGICAL & PHARMACEUTICAL BULLETIN, v.32, no.11, pp 1875 - 1879
- Pages
- 5
- Journal Title
- BIOLOGICAL & PHARMACEUTICAL BULLETIN
- Volume
- 32
- Number
- 11
- Start Page
- 1875
- End Page
- 1879
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13662
- DOI
- 10.1248/bpb.32.1875
- ISSN
- 0918-6158
1347-5215
- Abstract
- Interleukin (IL)-4 has been suggested as a molecular therapeutic target to prevent and/or treat various allergic diseases and several flavonoids have been Suggested as anti-allergic agents suppressing IL-4 production. In an effort to find novel candidates for anti-allergic agents from natural sources, we screened several flavonoids affecting on IL-4 production. In this study. we showed that 7,8,4'-trihydroxyflavone (T-412) significantly decreased IL-4 production both in phorbol 12-myristate 13-acetate (PMA) and ionomycin (PI)-activated EL-4 T cells and concanavalin A (ConA)-activated murine CD4(+) T cells in a dose- and time-dependent manner. The PI-induced increase of IL-4 mRNA expression was dramatically suppressed by T-412 at 6 h, indicating the suppression is regulated at transcriptional level. T-412 also significantly inhibited IL-4 gene promoter activity in EL-4 T cells transiently transfected with luciferase reporter plasmid containing IL-4 promoter (pGL4.14-IL.4). Western blot analysis of file transcription factors revealed that T-412 suppressed the nuclear expression of nuclear factor of. activated T cells (NF-AT)c1, c-Jun and c-Maf, but not c-Fos and nuclear factor kappa B (NF-kappa B). Our data suggested (hat T-412 might have potential as a candidate for anti-allergic agent having suppressive effects oil IL-4 production in activated T cells by controlling the transcription of IL-4.
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