Premium
Establishing the molecular modulation of the inflammation by xanthohumol and its metabolites in endothelial and smooth muscle cells
Author(s) -
Negrão Rita,
Moura Liane,
Soares Raquel
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.625.16
Subject(s) - xanthohumol , inflammation , umbilical vein , angiogenesis , chemistry , vascular smooth muscle , pharmacology , cell , biochemistry , microbiology and biotechnology , cancer research , immunology , biology , medicine , smooth muscle , ecology , key (lock) , in vitro
Vessel wall cells play relevant roles in inflammation. Xanthohumol (XN) and its metabolites isoxanthohumol (IXN) and 8‐prenylnaringenin (8PN) were described as anti‐inflammatory and anti‐angiogenic compounds. To understand the modulation of inflammation by these polyphenols in vessel walls, Human Umbilical Vein Endothelial Cells (HUVEC) and Human Aortic Smooth Muscle Cells (HASMC) were treated with 5‐10µM XN, IXN or 8PN for 24h. Expression profiles of angiogenic and inflammatory genes were examined by microarray assay. Genes involved in sprouting were down‐regulated by XN, IXN and increased by 8PN in HUVEC. Interleukin (IL)‐6 expression was increased in 8PN treatment. Conversely, HASMC increased TNFRSF12A after XN or 8PN incubation. XN and IXN downregulated IL‐12. Inflammatory responses in these cells were further evaluated measuring NO released (Griess reaction) and NFkB activity (ELISA) in cell nuclear extracts. A decrease in nitrite content was found for 8PN treatments. A reduction in NFkB activity was observed after treatment with XN and IXN, whereas 8PN incubation increased NFkB activity in both cell cultures.These findings reveal the distinct effects of these compounds in inflammation, providing clues to the development of useful therapeutic agents against inflammation‐ and angiogenesis‐associated pathologies. Funded by ERAB (EA0641) and FCT (SFRM/BD/41888/2007)