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Title: Deferiprone increases endothelial nitric oxide synthase phosphorylation and nitric oxide production
Authors: Thanaporn Sriwantana
Pornpun Vivithanaporn
Kittiphong Paiboonsukwong
Krit Rattanawonsakul
Sirada Srihirun
Nathawut Sibmooh
Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology;Medicine;Pharmacology, Toxicology and Pharmaceutics
Issue Date: 1-Jan-2018
Citation: Canadian Journal of Physiology and Pharmacology. Vol.96, No.9 (2018), 879-885
Abstract: © 2018, Canadian Science Publishing. All rights reserved. Iron chelation can improve endothelial function. However, effect on endothelial function of deferiprone has not been reported. We hypothesized deferiprone could promote nitric oxide (NO) production in endothelial cells. We studied effects of deferiprone on blood nitrite and blood pressure after single oral dose (25 mg/kg) in healthy subjects and hemoglobin E/β-thalassemia patients. Further, effects of deferiprone on NO production and endothelial NO synthase (eNOS) phosphorylation in primary human pulmonary artery endothelial cells (HPAEC) were investigated in vitro. Blood nitrite levels were higher in patients with deferiprone therapy than those without deferiprone (P = 0.023, n = 16 each). Deferiprone increased nitrite in plasma and whole blood of healthy subjects (P = 0.002 and 0.044) and thalassemia patients (P = 0.003 and 0.046) at time 180 min (n = 20 each). Asymptomatic reduction in diastolic blood pressure (P = 0.005) and increase in heart rate (P = 0.009) were observed in healthy subjects, but not in thalassemia patients. In HPAEC, deferiprone increased cellular nitrite and phospho-eNOS (Ser1177) (P = 0.012 and 0.035, n = 6) without alteration in total eNOS protein and mRNA. We conclude that deferiprone can induce NO production by enhancing eNOS phosphorylation in endothelial cells.
ISSN: 12057541
Appears in Collections:Scopus 2018

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