【摘 要】
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Oxidized low-density lipoprotein (Ox-LDL) is important in atherosclerosis in hyperlipidemia.Hematopoietic endothelial progenitor cells (EPCs) play an important role in preventing atherosclerosis, and
【机 构】
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Department of cardiology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Sha
【出 处】
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世界中医药学会联合会第二届老年医学专业委员会换届会暨2015学术年会
论文部分内容阅读
Oxidized low-density lipoprotein (Ox-LDL) is important in atherosclerosis in hyperlipidemia.Hematopoietic endothelial progenitor cells (EPCs) play an important role in preventing atherosclerosis, and notably decreased in hyperlipidemia.Ox-LDL and ox-LDL mediated reactive oxygen species (ROS) have deleterious effects on EPCs.On the other hand, probucol, as a powerful antioxidant and anti-inflammatory drug, could effectively reduce ROS production.This study was to explore if probucol could protect EPCs from ox-LDL in vivo and to investigate the potential mechanisms.Ox-LDL was used to inject into C57BL/6 mice for 3 days with or without probucol treatment.PBS was used as control.Bone marrow (BM) fluid, serum, hematopoietic mono nuclear cells (MCs) and EPCs were collected for test.Extracellular ROS in BM and blood as well as blood intracellular ROS production were significantly increased in male C57BL/6 mice with intravenous ox-LDL treatment.ROS formation was effectively blocked with probucol treatment.The elevated ox-LDL, C-reactive protein (CRP) and decreased superoxide dismutase (SOD) levels in hyperlipidemic patients were effectively reversed with probucol treatment.The diminished hematopoietic MCs and EPCs in mouse with ox-LDL treatment or in patients with high ox-LDL level were effectively recovered following probucol treatment.These data suggested that probucol was able to protect EPCs from ox-LDL through inhibition of ROS production.
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