Abstract 117: Heparin Derived Oligosaccharide Inhibits Vascular Intimal Hyperplasia in Balloon Injured Carotid Artery and the Mechanism Involved

Abstract

To determine the effects of heparin-derived oligosaccharides (HDOs) on vascular intimal hyperplasia (IH) in balloon-injured carotid artery and the mechanism involved. The animal model was established by rubbing the endothelia within the common carotid artery (CCA) of male rabbits along with a high-cholesterol diet. The arterial IH was testified by histopathological changes of the CCA. Serum lipids were detected using automated biochemical analysis; Expression of mRNAs corresponding to vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein-1 (MCP-1), scavenger receptor class B type I (SR-BI) and ATP-binding cassette transporter A1 (ABCA-1) were analyzed using reverse transcription polymerase chain reaction assays. Expressions of VEGF, VCAM-1, MCP-1, SR-BI and ABCA-1 proteins were detected by western blotting. Enzyme-linked immunosorbent assays were used to quantify expression levels of VEGF and bFGF. The results implied that administration of HDO significantly inhibited common carotid artery histopathology and restenosis that was induced by balloon injury. Treatment with HDO also significantly decreased mRNA and protein expression levels of VEGF, bFGF, VCAM-1, MCP-1, and SR-BI in the arterial wall, however ABCA-1 expression levels were elevated. HDO treatment led to a reduction in various serum lipids (total cholesterol, triglycerides, high-density and low-density lipoproteins). We concluded that, in a rabbit model, HDO can ameliorate IH and the mechanisms might involved VEGF, bFGF, VCAM-1, MCP-1, SR-BI and ABCA-1.