The Effect of AT1 Inhibitors on Pro-Inflammatory Cytokine Secretion By Human Coronary Endothelial Cells

Presentation Number: SUN 539
Date of Presentation: April 2nd, 2017

Krista Lucille Gonzales*1, Marilu Margarita Jurado-Flores2, Michael John Haas3, Ramadan Hammoud1, Kui-Tzu Feng1, Luisa M. Onstead-Haas1 and Arshag D Mooradian3
1University of Florida, Jacksonville, FL, 2University of Florida Health, Jacksonville, FL, 3University of Florida, Jacksonville, Jacksonville, FL


Background. Premature atherosclerosis associated with diabetes mellitus is associated with oxidative stress and inflammation.

Methods. To determine if high-dextrose affects expression of pro-inflammatory cytokines and if the effects are arrested by angiotensin 1 receptor inhibitors, human coronary artery endothelial cells (HCAEC) were exposed to either 5.5 mM or 27.5 mM dextrose for 24-hours with and without lisinopril, captopril, spironolactone, candesartan, and losartan in the conditioned medium.In addition, interleukin-1b (IL-1b), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor a (TNF a) levels were measured by enzyme-linked immunoassay.

Results. High-dextrose had no effect on IL-6 and IL-8 levels relative to cells exposed to 5.5 mM dextrose. In contrast, high-dextrose induced IL-1b levels significantly relative to cells exposed to 5.5 mM dextrose. Addition of lisinopril, captopril, spironolactone, losartan, and candesartan reduced IL-1b, IL-6, and IL-8 levels in cells exposed to both 5.5 mM and 27.5 mM dextrose. IL-2 and TNF a levels were below the level of detection under all conditions suggesting that HCAEC do not secrete these cytokines.

Conclusions. Inhibition of AT1 expression and/or activity reduced expression of several pro-inflammatory cytokines by HCAEC.


Nothing to Disclose: KLG, MMJ, MJH, RH, KTF, LMO, ADM