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conferenceseries
.com
Volume 9, Issue 5 (Suppl)
J Bioequiv Availab, an open access journal
ISSN: 0975-0851
Pharmacy & Biopharma 2017
August 31-September 01, 2017 Philadelphia, USA
August 31-September 01, 2017 Philadelphia, USA
3
rd
International Conference on
Biopharmaceutics and Biologic Drugs
&
5
th
International Pharmacy Conference
J Bioequiv Availab 2017, 9:5 (Suppl)
DOI: 10.4172/0975-0851-C1-031
Probucol protects endothelial progenitor cells against oxidized low-density lipoprotein via suppression of
reactive oxygen species formation
in vivo
Yuqi Cui
Ohio State University, USA
O
xidized 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. 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. 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. These data suggested that probucol could protect EPCs from Ox-LDL through inhibition of ROS
production
in vivo
.
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