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Ex vivo Effects of an Oenothera paradoxa Extract on the Reactive Oxygen Species Generation and Neutral Endopeptidase Activity in Neutrophils from Patients after Acute Myocardial Infarction
Author(s) -
Kiss Anna K.,
KapłonCieślicka Agnieszka,
Filipiak Krzysztof J.,
Opolski Grzegorz,
Naruszewicz Marek
Publication year - 2012
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3585
Subject(s) - reactive oxygen species , ex vivo , neprilysin , oxidative stress , myocardial infarction , superoxide , respiratory burst , mitochondrial ros , chemistry , biology , medicine , pharmacology , in vitro , immunology , biochemistry , enzyme
Oxidative stress induced by reactive oxygen species (ROS) is considered to play an important part in the aetiology of coronary heart disease. Apart from ROS, neutrophils are a source of neutral endopeptidase (NEP) that inactivates protective natriuretic peptides. The aim of the present study was to evaluate the in vitro ROS generation and inhibition of NEP activity in neutrophils obtained from healthy volunteers and from patients after acute myocardial infarction (AMI) by an aqueous extract of Oenothera paradoxa . Neutrophils isolated from AMI patients showed two‐fold higher ROS generation compared with cells from healthy donors, especially in the lucigenin‐enhanced luminescence model, which suggests intensive O ‐ 2 generation. The addition of O. paradoxa extract at concentrations of 0.2, 2 and 20 µg/mL resulted in a significant reduction in ROS generation. The extracellular NEP activity was higher in patients after AMI compared with healthy individuals (15.0 ± 0.9 versus 10.3 ± 0.5 nmol AMC/10 6 cells/60 min; p = 0.001). The addition of O. paradoxa extract at concentrations of 20, 50 and 100 µg/mL resulted in a significant reduction in NEP activity in both groups. O. paradoxa extract appears to be an interesting candidate for supplementation in the prevention of cardiovascular diseases. Copyright © 2011 John Wiley & Sons, Ltd.