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Flavonoids inhibit angiogenic cytokine production by human glioma cells
Author(s) -
Freitas Sandra,
Costa Silvia,
Azevedo Camila,
Carvalho Gerson,
Freire Songeli,
Barbosa Pedro,
Velozo Eudes,
Schaer Robert,
Tardy Marcienne,
Meyer Roberto,
Nascimento Ivana
Publication year - 2011
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3338
Subject(s) - angiogenesis , rutin , cytokine , bevacizumab , vascular endothelial growth factor , pharmacology , cell culture , cancer research , apigenin , monoclonal antibody , cell growth , chemistry , biology , medicine , flavonoid , antibody , immunology , vegf receptors , biochemistry , chemotherapy , antioxidant , genetics
VEGF and TGF‐β1 are cytokines that stimulate tissue invasion and angiogenesis. These factors are considered as molecular targets for the therapy of glioblastoma. Bevacizumab, a recombinant humanized monoclonal antibody developed against VEGF, inhibits endothelial cell proliferation and vessel formation. Flavonoids obtained from Dimorphandra mollis and Croton betulaster have been described as proliferation inhibitors of a human glioblastoma derived cell line. VEGF and TGF‐β1 levels were dosed by ELISA in a GL‐15 cell line treated with bevacizumab and also with the flavonoids rutin, 5‐hydroxy‐7,4′‐dimethoxyflavone, casticin, apigenin and penduletin. Rutin reduced the VEGF and TGF‐β1 levels after 24 h but not after 72 h. The other flavonoids significantly reduced TGF‐β1 production. Bevacizumab reduced only the VEGF levels in the supernatant from GL‐15 cultures. These results suggest that the flavonoids studied, and commonly used in popular medicine, present an interesting subject of study due to their potential effect as angiogenic factor inhibitors. Copyright © 2010 John Wiley & Sons, Ltd.