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dc.contributor.authorTykhomyrov, A.A. and Nedzvetsky, V.S. and Zabida, A.A. and Ağca, C.A. and Kuryata, O.V.
dc.date.accessioned2021-04-08T12:07:14Z
dc.date.available2021-04-08T12:07:14Z
dc.date.issued2018
dc.identifier10.1016/j.phanu.2018.06.005
dc.identifier.issn22134344
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85049529919&doi=10.1016%2fj.phanu.2018.06.005&partnerID=40&md5=9d79aaba5767ed4ac6f7096884ab0581
dc.identifier.urihttp://acikerisim.bingol.edu.tr/handle/20.500.12898/4264
dc.description.abstractL-Arginine is an important dietary amino acid with well-established role in cardiovascular health as a precursor of NO synthesis, however its effects on angiogenesis-related proteins in coronary artery disease (CAD) are not completely known. This study was undertaken to evaluate effects of L-arginine on the levels of key angiogenic regulators and matrix metalloproteinase (MMP) activity in sera of chronic heart failure (CHF) patients with CAD. Thirty-three patients were divided into two groups: 1) received only the standard treatment (control group, n = 13); 2) received L-arginine intravenous infusions in the dose of 4.2 g /100 mL for 7 days, followed by oral supplementation in the daily dose of 6 g for 3 months (n = 20). Significant up-regulation of vascular endothelial growth factor (VEGF) was found immunochemically in sera of L-arginine-treated patients as compared to control individuals. Serum MMP-2 and -9 activities were dramatically reduced after L-arginine treatment. Decrease in circulating levels of angiostatin and degradation products of fibronectin, a predominant constituent of the endothelial basement membrane, could result from L-arginine-induced inhibition of MMP activities. Our findings indicate that L-arginine rebounds the angiogenic balance in favour of improving neovascularization that potentially contributes to cardiovascular benefits in CHF patients with CAD. © 2018 Elsevier B.V.
dc.language.isoEnglish
dc.sourcePharmaNutrition
dc.titlel-Arginine treatment improves angiogenic response and reduces matrix metalloproteinase activity in chronic heart failure patients with coronary artery disease


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