Funded in part by 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 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Industry funded
- Company
- Amarin Corporation
- Company
- Amarin Pharma
Based on 2 listed funder(s).
Publication
- Published
- 2018-05-07 · Biomed Pharmacother · vol. 103 · pp. 1231–1237
- Publisher
- Elsevier BV
- Cited
- 84 citations · more than 95% of similar papers · 4.6× the field average
- Impact
- Top 10% most cited in its field
- References
- 80 works
- Access
- Open access (hybrid journal) · CC-BY
- Research areas
- Eicosanoids and Hypertension Pharmacology · Fatty Acid Research and Health · Cholesterol and Lipid Metabolism
- Keywords
- 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 authors
From US
- Richard Preston Mason · correspondingBrigham and Women's Hospital; Harvard University
- Hazem DawoudOhio University
- Robert Francis Jacob
- Samuel C. R. Sherratt
- Tadeusz MaliñskiOhio University
Abstract
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.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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