Cellular Physiology and Biochemistry (Jun 2016)

Probucol Protects Endothelial Progenitor Cells Against Oxidized Low-Density Lipoprotein via Suppression of Reactive Oxygen Species Formation In Vivo

  • Qingbin Zhang,
  • Liming Chen,
  • Zhihua Si,
  • Haoran Bu,
  • Chandrakala A. Narasimhulu,
  • Xueling Song,
  • Ming-Yu Cui,
  • Hang Liu,
  • Tiewei Lu,
  • Guanglong He,
  • Sampath Parthasarathy,
  • Lianqun Cui,
  • Zhenguo Liu,
  • Yuqi Cui

DOI
https://doi.org/10.1159/000445608
Journal volume & issue
Vol. 39, no. 1
pp. 89 – 101

Abstract

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Background/Aims: Oxidized low-density lipoprotein (ox-LDL) is a major component of hyperlipidemia and contributes to atherosclerosis. Endothelial progenitor cells (EPCs) play an important role in preventing atherosclerosis and notably decreased in hyperlipidemia. Ox-LDL and ox-LDL-related reactive oxygen species (ROS) have deleterious effects on EPCs. Probucol as an antioxidant and anti-inflammatory drug reduces ROS production. The present study was to determine if probucol could protect EPCs from ox-LDL in vivo and to investigate the potential mechanisms. Methods: ox-LDL was injected into male C57BL/6 mice for 3 days with or without probucol treatment with PBS as control. Bone marrow (BM) fluid, serum, circulating mononuclear cells (MNCs) and EPCs were collected for analysis. Results: the increased extracellular ROS in BM, serum and blood intracellular ROS production in the mice with ox-LDL treatment in association with a significant reduction of circulating MNCs and EPCs were restored with Probucol treatment. A significant increase in the serum ox-LDL and C-reactive protein and decrease in superoxide dismutase and circulating MNCs and EPCs were observed in hyperlipidemic patients that were effectively reversed with probucol treatment. Conclusion: these data suggested that probucol could protect EPCs from ox-LDL through inhibition of ROS production in vivo.

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