Eicosapentaenoic acid inhibits oxidation of high density lipoprotein particles in a manner distinct from docosahexaenoic acid
Sherratt SCR, Mason RP
Biochemical and biophysical research communications · 40 citas
Etiquetas de revisión
Financiación no declaradaSolo 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
- Financiación no declarada
Publicación
- Publicado
- 2018-01-10 · Biochem Biophys Res Commun · vol. 496 · número 2 · págs. 335–338
- Editorial
- Elsevier BV
- Citado
- 50 citas · más que el 90% de estudios similares · 2.7× el promedio de su campo
- Referencias
- 31 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY-NC-ND
- Áreas de investigación
- Fatty Acid Research and Health · Eicosanoids and Hypertension Pharmacology · Antioxidant Activity and Oxidative Stress
- Palabras clave
- Eicosapentaenoic acid, Antioxidant, Docosahexaenoic acid, Hypertriglyceridemia, Chemistry, Lipoprotein, Biochemistry, Apolipoprotein B, Lipid peroxidation, Triglyceride, Fatty acid, Internal medicine, Cholesterol, Polyunsaturated fatty acid, Medicine
- MeSH
- humans, copper, docosahexaenoic acids, eicosapentaenoic acid, triglycerides, lipoproteins, hdl, antioxidants, centrifugation, density gradient, oxidation-reduction
2 autores
- Samuel C. R. Sherratt
- Richard Preston Mason🇺🇸 · autor de correspondenciaBrigham and Women's Hospital; Harvard University
Resumen
El texto original del estudio, en el idioma en que se publicó.
The omega-3 fatty acid eicosapentaenoic acid (EPA) reduces oxidation of ApoB-containing particles in vitro and in patients with hypertriglyceridemia. EPA may produce these effects through a potent antioxidant mechanism, which may facilitate LDL clearance and slow plaque progression. We hypothesize that EPA antioxidant effects may extend to ApoA-containing particles like HDL, potentially preserving certain atheroprotective functions. HDL was isolated from human plasma and incubated at 37 °C in the absence (vehicle) or presence of EPA and/or DHA; 5.0 or 10.0 μM each. Samples were then subjected to copper-induced oxidation (10 μM). HDL oxidation was inhibited similarly by EPA and DHA up to 1 h. EPA (10 μM) maintained significant HDL oxidation inhibition of 89% (0.622 ± 0.066 μM MDA; p < .001) at 4 h, with continued inhibition of 64% at 14 h, vs. vehicle (5.65 ± 0.06 to 2.01 ± 0.10 μM MDA; p < .001). Conversely, DHA (10 μM) antioxidant benefit was lost by 4 h. At a lower concentration (5 μM), EPA antioxidant activity remained at 81% (5.53 ± 0.15 to 1.03 ± 0.10 μM MDA; p < .001) at 6 h, while DHA lost all antioxidant activity by 4 h. The antioxidant activity of EPA was preserved when combined with an equimolar concentration of DHA (5 μM each). EPA pretreatment prevented HDL oxidation in a dose-dependent manner that was preserved over time. These results suggest unique lipophilic and electron stabilization properties for EPA as compared to DHA with respect to inhibition of HDL oxidation. These antioxidant effects of EPA may enhance certain atheroprotective functions for HDL.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY-NC-ND).
Confianza de la comunidad
Cargando…
¿Cuánto confías en los hallazgos de este estudio?
Comentarios
¿Algo está mal aquí?
Señala este estudio si su información, etiquetas o financiación parecen incorrectas. Un editor revisa cada señalamiento.
Información educativa sobre investigación publicada. No es consejo médico ni una recomendación para empezar o dejar nada.