Attila Zalatnai1, Ferenc Timár. 1. First Department of Pathology and Experimental Cancer Research, Semmelweis University, Faculty of Medicine, H-1085 Budapest, Hungary. zalatnai@korbl.sote.hu
Abstract
BACKGROUND: The somatostatin analog octreotide (Sandostatin) exerts its antineoplastic effect through different mechanisms. There are several in vitro and in vivo studies available demonstrating an antiangiogenic activity, however, some other observations failed to reinforce these results. We investigated the potential angio-inhibiting activity of this drug in an in vitro system using human placental fragments. MATERIALS AND METHODS: In an in vitro angiogenesis assay, small pieces of human placenta were embedded in a fibrin gel and the effect of 1, 10 and 100 micrograms/ml Sandostatin was assessed on the microvessel formation. The results were expressed as microvessel counts per mm perimeter. RESULTS: At a dose of 1 microgram/mL octreotide did not influence the microvessel outgrowth, however, a 10 micrograms/ml concentration resulted in a 61% inhibition, while in the samples treated with 100 micrograms/ml Sandostatin only occasional capillary tubes formed. CONCLUSION: Sandostatin effectively inhibited the outgrowth of the placental vessels in a dose-dependent manner. In the mechanism of action of this drug the antiangiogenic effect should also be taken into account.
BACKGROUND: The somatostatin analog octreotide (Sandostatin) exerts its antineoplastic effect through different mechanisms. There are several in vitro and in vivo studies available demonstrating an antiangiogenic activity, however, some other observations failed to reinforce these results. We investigated the potential angio-inhibiting activity of this drug in an in vitro system using human placental fragments. MATERIALS AND METHODS: In an in vitro angiogenesis assay, small pieces of human placenta were embedded in a fibrin gel and the effect of 1, 10 and 100 micrograms/ml Sandostatin was assessed on the microvessel formation. The results were expressed as microvessel counts per mm perimeter. RESULTS: At a dose of 1 microgram/mL octreotide did not influence the microvessel outgrowth, however, a 10 micrograms/ml concentration resulted in a 61% inhibition, while in the samples treated with 100 micrograms/ml Sandostatin only occasional capillary tubes formed. CONCLUSION:Sandostatin effectively inhibited the outgrowth of the placental vessels in a dose-dependent manner. In the mechanism of action of this drug the antiangiogenic effect should also be taken into account.