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Chrysin, Apigenin and Acacetin Inhibit Tumor Necrosis Factor-Related Apoptosis—Inducing Ligand Receptor-1 (TRAIL-R1) on Activated RAW264.7 Macrophages
- Source :
- International Journal of Molecular Sciences, Volume 15, Issue 7, Pages 11510-11522, International Journal of Molecular Sciences, Vol 15, Iss 7, Pp 11510-11522 (2014)
- Publication Year :
- 2014
- Publisher :
- Multidisciplinary Digital Publishing Institute, 2014.
-
Abstract
- 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.
- Subjects :
- Receptor expression
Flavones
Article
Catalysis
Cell Line
lcsh:Chemistry
Inorganic Chemistry
Mice
chemistry.chemical_compound
chrysin
acacetin
Animals
Chrysin
Physical and Theoretical Chemistry
Receptor
lcsh:QH301-705.5
Molecular Biology
Spectroscopy
Flavonoids
chemistry.chemical_classification
apigenin
Acacetin
Macrophages
Organic Chemistry
General Medicine
RAW264.7
Computer Science Applications
TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)-receptor (TRAIL-R) expression
Receptors, TNF-Related Apoptosis-Inducing Ligand
lcsh:Biology (General)
lcsh:QD1-999
chemistry
Biochemistry
Apoptosis
Apigenin
Cancer research
Tumor necrosis factor alpha
Subjects
Details
- Language :
- English
- ISSN :
- 14220067
- Database :
- OpenAIRE
- Journal :
- International Journal of Molecular Sciences
- Accession number :
- edsair.doi.dedup.....3deecd5627a01ba9569f67c8b637af37
- Full Text :
- https://doi.org/10.3390/ijms150711510