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Open Access Research article

Stilbene glycosides are natural product inhibitors of FGF-2-induced angiogenesis

Sajjad Hussain1, Mark Slevin2, Nessar Ahmed2, David West3, Muhammad Iqbal Choudhary4, Humera Naz4 and John Gaffney2*

Author affiliations

1 Department of Paediatrics and Adolescent Medicine, Mayo Clinic, Rochester, MN 55902, USA

2 School of Chemistry, Biology and Health Sciences, Manchester Metropolitan University, Chester St, Manchester, M1 5GD, UK

3 School of Biological Sciences, University of Liverpool, Liverpool, L69 7ZB, UK

4 HEJ Research Institute of Chemistry, International Centre for Biological and Chemical Sciences, University of Karachi, Karachi 75720, Pakistan

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Citation and License

BMC Cell Biology 2009, 10:30  doi:10.1186/1471-2121-10-30

Published: 23 April 2009



Angiogenesis, the growth of new blood vessels from the pre-existing vasculature is associated with pathological processes, in particular tumour development, and is a target for the development of new therapies. We have investigated the anti-angiogenic potential of two naturally occurring stilbene glycosides (compounds 1 and 2) isolated from the medicinal plant Boswellia papyriferai using large and smallvessel-derived endothelial cells. Compound 1 (trans-4',5'-dihydroxy-3-methoxystilbene-5-O-{α-L-rhamnopyranosyl-(1→2)-[α-L-rhamnopyranosyl-(1→6)}-β-D-glucopyranoside was the more hydrophilic and inhibited FGF-2-induced proliferation, wound healing, invasion in Matrigel, tube formation and angiogenesis in large and small vessel-derived endothelial cells and also in the chick chorioallantoic membrane assay. Using a binding assay we were able to show compound 1 reduced binding of FGF-2 to fibroblast growth factor receptors-1 and -2. In all cases the concentration of compound 1 which caused 50% inhibition (IC50) was determined. The effect of compound 1 on EGF and VEGF-induced proliferation was also investigated.


Compound 1 inhibited all stages of FGF-2 induced angiogenesis with IC50 values in the range 5.8 ± 0.18 – 48.90 ± 0.40 μM but did not inhibit EGF or VEGF-induced angiogenesis. It also inhibited FGF-2 binding to FGF receptor-1 and -2 with IC50 values of 5.37 ± 1.04 and 9.32 ± 0.082 μM respectively and with concommotant down-regulation of phosphorylated-ERK-1/-2 expression. Compound 2 was an ineffective inhibitor of angiogenesis despite its structural homology to compound 1.


Compound 1 inhibited FGF-2 induced angiogenesis by binding to its cognate receptors and is an addition to the small number of natural product inhibitors of angiogenesis