Heparin-derived oligosaccharide inhibits vascular intimal hyperplasia in balloon-injured carotid artery.
10.1016/S1875-5364(17)30066-3
- Author:
Jie-Ru LIU
1
;
Jie WU
1
;
Xin-Chao YU
1
;
Xuan QIAN
1
;
Rui XIONG
1
;
Hui-Fang WANG
1
;
Dan-Feng YU
1
;
Fei-Fei LIU
1
;
Shu-Ying HE
2
Author Information
1. School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China.
2. School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China. Electronic address: heshuying92@126.com.
- Publication Type:Journal Article
- Keywords:
Atherosclerosis;
Balloon injury;
Heparin-derived oligosaccharide;
Intimal hyperplasia
- MeSH:
ATP Binding Cassette Transporter 1;
analysis;
Animals;
Carotid Artery Injuries;
drug therapy;
pathology;
Chemokine CCL2;
analysis;
Heparin;
therapeutic use;
Hyperplasia;
Male;
Oligosaccharides;
therapeutic use;
Rabbits;
Tunica Intima;
pathology;
Vascular Cell Adhesion Molecule-1;
analysis;
Vascular Endothelial Growth Factor A;
analysis
- From:
Chinese Journal of Natural Medicines (English Ed.)
2017;15(6):442-450
- CountryChina
- Language:English
-
Abstract:
The aims of the present study were to determine the effects of heparin-derived oligosaccharides (HDOs) on vascular intimal hyperplasia (IH) in balloon-injured carotid artery and to elucidate the underlying mechanisms of action. An animal model was established by rubbing the endothelia within the common carotid artery (CCA) in male rabbits. The rabbits were fed a high-cholesterol diet. Arterial IH was determined by histopathological changes to the CCA. Serum lipids were detected using an automated biochemical analysis. Expressions of mRNAs for 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 analyzed by Western blotting. Enzyme-linked immunosorbent assays were used to quantify expression levels of VEGF and bFGF. Our results showed that administration of HDO significantly inhibited CCA histopathology and restenosis induced by balloon injury. The treatment with HDOs significantly decreased the mRNA and protein expression levels of VEGF, bFGF, VCAM-1, MCP-1, and SR-BI in the arterial wall; however, ABCA-1 expression level was elevated. HDO treatment led to a reduction in serum lipids (total cholesterol, triglycerides, high-density and low-density lipoproteins). Our results from the rabbit model indicated that HDOs could ameliorate IH and underlying mechanism might involve VEGF, bFGF, VCAM-1, MCP-1, SR-BI, and ABCA-1.
