期刊论文详细信息
International Journal of Molecular Sciences
Chrysin, Apigenin and Acacetin Inhibit Tumor Necrosis Factor-Related Apoptosis—Inducing Ligand Receptor-1 (TRAIL-R1) on Activated RAW264.7 Macrophages
Monika Warat2  Ewelina Szliszka2  Ilona Korzonek-Szlacheta1  Wojciech Król2 
[1] Department of Toxicology and Health Protection, Toxicology and Drug Addiction Division, Medical University of Silesia in Katowice, Medyków 18, 40-752 Katowice, Poland; E-Mail:;Chair and Department of Microbiology and Immunology, Medical University of Silesia in Katowice, Jordana 19, 41-808 Zabrze, Poland; E-Mails:
关键词: chrysin;    apigenin;    acacetin;    TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)-receptor (TRAIL-R) expression;    RAW264.7;   
DOI  :  10.3390/ijms150711510
来源: mdpi
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【 摘 要 】

Expression level of Tumor Necrosis Factor—related apoptosis—inducing ligand (TRAIL) receptors is one of the most important factors of TRAIL-mediated apoptosis in cancer cells. We here report for the first time data concerning TRAIL-R1 and TRAIL-R2 receptor expression on RAW264.7 macrophages. Three substances belonging to flavones: chrysin, apigenin and acacetin which differ from their substituents at the 4' position in the phenyl ring were used in assays because of the variety of biological activities (e.g., anticancer activity) of the polyphenol compounds. The expression of TRAIL-R1 and TRAIL-R2 death receptors on non-stimulated and LPS (lipopolysaccharide)-stimulated macrophages was determined using flow cytometry. We demonstrate that RAW264.7 macrophages exhibit TRAIL-R1 surface expression and that the tested compounds: chrysin, apigenin and acacetin can inhibit TRAIL-R1 death receptor expression level on macrophages.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.

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