Arctigenin from Arctium lappa inhibits interleukin-2 and interferon gene expression in primary human T lymphocytes
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- 作者：Wei-Jern Tsai (1)
Chu-Ting Chang (2)
Guei-Jane Wang (1)
Tzong-Huei Lee (3)
Shwu-Fen Chang (4)
Shao-Chun Lu (5)
Yuh-Chi Kuo (2) - 刊名：Chinese Medicine
- 出版年：2011
- 出版时间：December 2011
- 年：2011
- 卷：6
- 期：1
- 全文大小：463KB
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Chu-Ting Chang (2)
Guei-Jane Wang (1)
Tzong-Huei Lee (3)
Shwu-Fen Chang (4)
Shao-Chun Lu (5)
Yuh-Chi Kuo (2)
1. National Research Institute of Chinese Medicine, Taipei, 11221, Taiwan
2. Institute of Life Science, Fu-Jen University, Taipei, 24205, Taiwan
3. Graduate Institute of Pharmacology Science, Taipei Medical University, Taipei, 11031, Taiwan
4. Graduate Institute of Medical Sciences, Taipei Medical University, Taipei, 11031, Taiwan
5. Department of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, Taipei, 10051, Taiwan
文摘
Background Arctium lappa (Niubang), a Chinese herbal medicine, is used to treat tissue inflammation. This study investigates the effects of arctigenin (AC), isolated from A. lappa, on anti-CD3/CD28 Ab-stimulated cell proliferation and cytokine gene expression in primary human T lymphocytes. Methods Cell proliferation was determined with enzyme immunoassays and the tritiated thymidine uptake method. Cytokine production and gene expression were analyzed with reverse transcription-polymerase chain reaction. Results AC inhibited primary human T lymphocytes proliferation activated by anti-CD3/CD28 Ab. Cell viability test indicated that the inhibitory effects of AC on primary human T lymphocyte proliferation were not due to direct cytotoxicity. AC suppressed interleukin-2 (IL-2) and interferon-γ (IFN-γ) production in a concentration-dependent manner. Furthermore, AC decreased the IL-2 and IFN-γ gene expression in primary human T lymphocytes induced by anti-CD3/CD28 Ab. Reporter gene analyses revealed that AC decreased NF-AT-mediated reporter gene expression. Conclusion AC inhibited T lymphocyte proliferation and decreased the gene expression of IL-2, IFN-γ and NF-AT.