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      Heparin-derived oligosaccharide inhibits vascular intimal hyperplasia in balloon-injured carotid artery

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          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.

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          Author and article information

          Journal
          CJNM
          Chinese Journal of Natural Medicines
          Elsevier
          1875-5364
          20 June 2017
          : 15
          : 6
          : 442-450
          Affiliations
          1School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China
          Author notes
          *Corresponding author: HE Shu-Ying, Tel/Fax: 86-25-83271249, E-mail: heshuying92@ 123456126.com

          These authors have no conflict of interest to declare.

          Article
          S1875-5364(17)30066-3
          10.1016/S1875-5364(17)30066-3
          Copyright © 2017 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
          Funding
          Funded by: National Basic Research Funds
          Award ID: JKYJ2013044
          Funded by: National Basic Research Funds
          Award ID: JKZ2011013
          Funded by: National Science and Technology Project of China
          Award ID: 2012ZX09502001-004
          This work was supported by the National Basic Research Funds (Nos. JKYJ2013044 and JKZ2011013), the Significant New Drugs Innovation Support Program of the National Science and Technology Project of China (No. 2012ZX09502001-004), and the Priority Academic Program Development of Jiangsu Higher Education Institution.

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