Dysfunction of endothelial progenitor cells in hyperlipidemic rats involves the increase of NADPH oxidase derived reactive oxygen species production.
Can J Physiol Pharmacol
; 95(5): 474-480, 2017 May.
Article
em En
| MEDLINE
| ID: mdl-28177697
ABSTRACT
NADPH oxidase (NOX) is a major source of reactive oxygen species (ROS) in the body and it plays a key role in mediation of oxidative injury in the cardiovascular system. The purposes of this study are to evaluate the status of NOX in endothelial progenitor cells (EPCs) of hyperlipidemic rats and to determine whether NOX-derived ROS promotes the dysfunction of EPCs. The rats were fed on a high-fat diet for 8 weeks to establish a hyperlipidemic rat model, which showed the increased plasma lipids and the impaired functions of circulating EPCs (including the reduced abilities in migration and adhesion) accompanied by an increase in NOX activity and ROS production. Next, EPCs were isolated from normal rats and they were treated with oxidized low-density lipoprotein (ox-LDL) (100 µg/mL) for 24 h to induce a dysfunctional model in vitro. In agreement with our findings in vivo, ox-LDL treatment increased the dysfunctions of EPCs concomitant with an increase in NOX activity and ROS production; these phenomena were reversed by the NOX inhibitor. Based on these observations, we conclude that NOX-derived ROS involved in the dysfunctions of circulating EPCs in hyperlipidemic rats and inhibition of NOX might provide a novel strategy to improve EPC functions in hyperlipidemia.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Espécies Reativas de Oxigênio
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NADPH Oxidases
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Células Progenitoras Endoteliais
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Hiperlipidemias
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Can J Physiol Pharmacol
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
China