Financiado en parte por Amarin Corporation, Amarin Pharma
Eicosapentaenoic acid improves endothelial function and nitric oxide bioavailability in a manner that is enhanced in combination with a statin
Mason RP, Dawoud H, Jacob RF, Sherratt SCR, Malinski T
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 64 citas
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Financiado por la industriaSolo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Células o muestras de laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiado por la industria
- Empresa
- Amarin Corporation
- Empresa
- Amarin Pharma
Según 2 financiadores declarados.
Publicación
- Publicado
- 2018-05-07 · Biomed Pharmacother · vol. 103 · págs. 1231–1237
- Editorial
- Elsevier BV
- Citado
- 84 citas · más que el 95% de estudios similares · 4.6× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 80 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY
- Áreas de investigación
- Eicosanoids and Hypertension Pharmacology · Fatty Acid Research and Health · Cholesterol and Lipid Metabolism
- Palabras clave
- Eicosapentaenoic acid, Nitric oxide, Endothelial dysfunction, Pharmacology, Oxidative stress, Fenofibrate, Endothelial stem cell, Chemistry, Docosahexaenoic acid, Peroxynitrite, Vasoprotective, Endothelium, Umbilical vein, Biochemistry, Endothelial progenitor cell, Niacin, Apocynin, Human umbilical vein endothelial cell, Superoxide, Endocrinology, Medicine, Fatty acid, NADPH oxidase, Polyunsaturated fatty acid, In vitro
- MeSH
- endothelium, vascular, animals, rats, inbred wky, humans, nitric oxide, eicosapentaenoic acid, lipoproteins, ldl, hydroxymethylglutaryl-coa reductase inhibitors, biological availability, kinetics, male, human umbilical vein endothelial cells, atorvastatin
5 autores
- Richard Preston Mason🇺🇸 · autor de correspondenciaBrigham and Women's Hospital; Harvard University
- Hazem Dawoud🇺🇸Ohio University
- Robert Francis Jacob
- Samuel C. R. Sherratt
- Tadeusz Maliñski🇺🇸Ohio University
Resumen
El texto original del estudio, en el idioma en que se publicó.
The endothelium exerts many vasoprotective effects that are largely mediated by release of nitric oxide (NO). Endothelial dysfunction represents an early but reversible step in atherosclerosis and is characterized by a reduction in the bioavailability of NO. Previous studies have shown that eicosapentaenoic acid (EPA), an omega-3 fatty acid (O3FA), and statins individually improve endothelial cell function, but their effects in combination have not been tested. Through a series of in vitro experiments, this study evaluated the effects of a combined treatment of EPA and the active metabolite of atorvastatin (ATM) on endothelial cell function under conditions of oxidative stress. Specifically, the comparative and time-dependent effects of these agents on endothelial dysfunction were examined by measuring the levels of NO and peroxynitrite (ONOO-) released from human umbilical vein endothelial cells (HUVECs). The data suggest that combined treatment with EPA and ATM is beneficial to endothelial function and was unique to EPA and ATM since similar improvements could not be recapitulated by substituting another O3FA docosahexaenoic acid (DHA) or other TG-lowering agents such as fenofibrate, niacin, or gemfibrozil. Comparable beneficial effects were observed when HUVECs were pretreated with EPA and ATM before exposure to oxidative stress. Interestingly, the kinetics of EPA-based protection of endothelial function in response to oxidation were found to be significantly different than those of DHA. Lastly, the beneficial effects on endothelial function generated by combined treatment of EPA and ATM were reproduced when this study was expanded to an ex vivo model utilizing rat glomerular endothelial cells. Taken together, these findings suggest that a combined treatment of EPA and ATM can inhibit endothelial dysfunction that occurs in response to conditions such as hyperglycemia, oxidative stress, and dyslipidemia.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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