Premium
Effects of Gelidium amansii on the cell proliferation and markers of angiogenesis in endothelial EA hy 926 cells
Author(s) -
Chang HsiaoPei,
Chen YueHwa
Publication year - 2006
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.20.4.a566-b
Subject(s) - angiogenesis , chemistry , endothelial stem cell , cell growth , vascular endothelial growth factor , matrix metalloproteinase , phorbol , in vitro , cell , secretion , biochemistry , cell culture , microbiology and biotechnology , biology , vegf receptors , enzyme , protein kinase c , cancer research , genetics
The objective of this study was to investigate the effects of Gelidium amansii (GA), an edible red agar cultivated off the northeast coast of Taiwan, on the cell proliferation and in vitro markers of angiogenesis in endothelial EA hy 926 cells. Both phosphate‐buffered saline (PBS) and methanol extracts from dried GA powder were prepared and utilized for treatment. The results showed that a high concentration of PBS extract (7.5mg/mL) inhibited cell growth and proliferation in both phorbol myristate acetate (PMA)‐treated and PMA‐untreated cells, whereas methanol extract showed no such inhibitory effect. Parallel to the results obtained from cell growth and proliferation, PBS extract (7.5 mg/mL) also inhibited PMA‐induced tube formation. Additionally, PMA‐stimulated vascular endothelial growth factor (VEGF) secretion was also inhibited by the treatment of PBS extracts (2.5~7.5 mg/mL). Nevertheless, neither PBS nor methanol extracts affected matrix metalloproteinase‐2 (MMP‐2) activity. These results suggested that water‐soluble (PBS) fraction of GA inhibited PMA‐stimulated cell proliferation, tube formation, and VEGF secretion, which are factors associated with angiogenesis. Although lipid‐soluble fraction of GA did not show such inhibitory effects, consumption of GA may be useful in the treatment human cancer and angiogenesis‐related diseases. (Supported by DOH grant DOH93‐TD‐F‐113‐049‐(2))