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Cardiovascular effects of resveratrol and atorvastatin treatments in an H(2)O(2)-induced stress model

Oxidative stress has been implicated in the pathophysiology of several types of cardiovascular disease (CVD). Statins are widely used to inhibit the progression of atherosclerosis and reduce the incidence of CVD. Certain over-the-counter products, including resveratrol, show similar effects to stati...

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Autores principales: SONER, BURAK CEM, ŞAHIN, AYŞE SAIDE
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186369/
https://www.ncbi.nlm.nih.gov/pubmed/25289077
http://dx.doi.org/10.3892/etm.2014.1956
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author SONER, BURAK CEM
ŞAHIN, AYŞE SAIDE
author_facet SONER, BURAK CEM
ŞAHIN, AYŞE SAIDE
author_sort SONER, BURAK CEM
collection PubMed
description Oxidative stress has been implicated in the pathophysiology of several types of cardiovascular disease (CVD). Statins are widely used to inhibit the progression of atherosclerosis and reduce the incidence of CVD. Certain over-the-counter products, including resveratrol, show similar effects to statins and may thus be used in conjunction with statins for the treatment of the majority of patients with CVD. The aim of the present study was to evaluate the effects of atorvastatin, resveratrol and resveratrol + atorvastatin (R+A) pretreatment on myocardial contractions and vascular endothelial functions in the presence of H(2)O(2) as an experimental model of oxidative stress in rats. Four groups were established and referred to as the control, atorvastatin, resveratrol and R+A groups. Atorvastatin (40 mg/kg, per oral) and/or resveratrol (30 mg/kg, intraperitoneal) treatments were administered for 14 days. On the 15th day, the thoracic aortas and hearts of the rats were dissected and placed into isolated organ baths. Vascular responses to cumulative doses of H(2)O(2) (1×10(−8)–1×10(−4) M H(2)O(2)) with and without N (G)-nitro-L-arginine methyl ester (L-NAME) incubation were measured. In addition, myocardial electrical stimulation (ES) responses to various H(2)O(2) concentrations (1×10(−7)–1×10(−5) M H(2)O(2)) were evaluated. In the control and atorvastatin groups, H(2)O(2) application caused a significant dose-dependent decrease in the ES-induced contractions in the myocardial tissue of rats. In the resveratrol and R+A groups, H(2)O(2) application did not significantly affect myocardial contraction at any dose. In all groups, incubation with L-NAME caused a significant augmentation in the H(2)O(2) response, revealing that this effect was mediated via the vascular endothelium. In conclusion, pretreatment with R+A for CVD appears to be superior to pretreatment with either agent alone.
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spelling pubmed-41863692014-10-06 Cardiovascular effects of resveratrol and atorvastatin treatments in an H(2)O(2)-induced stress model SONER, BURAK CEM ŞAHIN, AYŞE SAIDE Exp Ther Med Articles Oxidative stress has been implicated in the pathophysiology of several types of cardiovascular disease (CVD). Statins are widely used to inhibit the progression of atherosclerosis and reduce the incidence of CVD. Certain over-the-counter products, including resveratrol, show similar effects to statins and may thus be used in conjunction with statins for the treatment of the majority of patients with CVD. The aim of the present study was to evaluate the effects of atorvastatin, resveratrol and resveratrol + atorvastatin (R+A) pretreatment on myocardial contractions and vascular endothelial functions in the presence of H(2)O(2) as an experimental model of oxidative stress in rats. Four groups were established and referred to as the control, atorvastatin, resveratrol and R+A groups. Atorvastatin (40 mg/kg, per oral) and/or resveratrol (30 mg/kg, intraperitoneal) treatments were administered for 14 days. On the 15th day, the thoracic aortas and hearts of the rats were dissected and placed into isolated organ baths. Vascular responses to cumulative doses of H(2)O(2) (1×10(−8)–1×10(−4) M H(2)O(2)) with and without N (G)-nitro-L-arginine methyl ester (L-NAME) incubation were measured. In addition, myocardial electrical stimulation (ES) responses to various H(2)O(2) concentrations (1×10(−7)–1×10(−5) M H(2)O(2)) were evaluated. In the control and atorvastatin groups, H(2)O(2) application caused a significant dose-dependent decrease in the ES-induced contractions in the myocardial tissue of rats. In the resveratrol and R+A groups, H(2)O(2) application did not significantly affect myocardial contraction at any dose. In all groups, incubation with L-NAME caused a significant augmentation in the H(2)O(2) response, revealing that this effect was mediated via the vascular endothelium. In conclusion, pretreatment with R+A for CVD appears to be superior to pretreatment with either agent alone. D.A. Spandidos 2014-11 2014-09-11 /pmc/articles/PMC4186369/ /pubmed/25289077 http://dx.doi.org/10.3892/etm.2014.1956 Text en Copyright © 2014, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
SONER, BURAK CEM
ŞAHIN, AYŞE SAIDE
Cardiovascular effects of resveratrol and atorvastatin treatments in an H(2)O(2)-induced stress model
title Cardiovascular effects of resveratrol and atorvastatin treatments in an H(2)O(2)-induced stress model
title_full Cardiovascular effects of resveratrol and atorvastatin treatments in an H(2)O(2)-induced stress model
title_fullStr Cardiovascular effects of resveratrol and atorvastatin treatments in an H(2)O(2)-induced stress model
title_full_unstemmed Cardiovascular effects of resveratrol and atorvastatin treatments in an H(2)O(2)-induced stress model
title_short Cardiovascular effects of resveratrol and atorvastatin treatments in an H(2)O(2)-induced stress model
title_sort cardiovascular effects of resveratrol and atorvastatin treatments in an h(2)o(2)-induced stress model
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186369/
https://www.ncbi.nlm.nih.gov/pubmed/25289077
http://dx.doi.org/10.3892/etm.2014.1956
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