Abstract 13892: Purified Eicosapentaenoic Acid Ameliorates Cardiac Fibrosis and Tissue Inflammation in Spontaneously Hypertensive Rats

• Published in: Circulation (New York, N.Y.) Vol. 140; no. Suppl_1 Suppl 1; p. A13892
• Main Authors: Melendez, Giselle C, Medina-Hernandez, Danielle, Pflum, Adam W, Xu, Vivian, Herrington, David M
• Format: Journal Article
• Language: English
• Published: by the American College of Cardiology Foundation and the American Heart Association, Inc 19.11.2019
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.140.suppl_1.13892

IntroductionWe have previously shown that eicosapentaenoic acid (EPA) treatment decreases left ventricular (LV) diastolic dysfunction and interstitial cardiac fibrosis in rats with established hypertension. Evidence suggests that these beneficial effects may be related to the anti-inflammatory properties of EPA. We sought to determine whether purified EPA consumption mitigates LV immune cell recruitment and pro-inflammatory cytokines levels in hypertensive rats.MethodsThirty 12 week-old spontaneously hypertensive rats (SHR) were randomized to receive purified EPA or corn oil supplemented diet (Control [CTL]) for 20 weeks. At experimental endpoint, we assessed in a blinded analysis tail-cuff systolic blood pressures (SBP). Animals were euthanized to measure LV collagen volume fraction (CVF) by picrosirius red stain, mast cell density by toluidine blue stain and macrophages numbers by immunohistochemistry. Eight LV cytokines and growth factors were measured by ELISA.ResultsEPA diet did not have an effect on SBP (p=0.56). Rats on EPA diet had lower CVF (EPA1.62 ± 0.07 % vs. CTL2.43 ± 0.01 %; p<0.0001). EPA had no effect on cardiac mast cell density (CTL0.91 ± 0.20 vs EPA0.73 ± 0.06, p=0.2), however, it decreased LV macrophages numbers per microscopy field (CTL26.8 ± 2.5 vs. 18.5 ± 2.5, p=0.01) and increased interleukin (IL-)10 (CTL64.2 ± 3.9 pg/mL vs. EPA73.7 ± 4.0 pg/mL, p=0.05)(Figure).ConclusionsHypertensive animals on an EPA enriched diet exhibited a decreased LV macrophage recruitment and up-regulation of the anti-inflammatory cytokine IL-10. These results suggest that the anti-fibrotic effects of EPA may be due to the suppression of inflammatory cell recruitment and production of protective cytokines in the myocardium, and not to the suppression of pro-inflammatory cytokines. Future studies are needed to establish causation between these anti-inflammatory effects of EPA and mitigation of cardiac fibrosis.