Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2018 (2018), Article ID 8237209, 11 pages
https://doi.org/10.1155/2018/8237209
Research Article

Analysis of Drug Effects on Primary Human Coronary Artery Endothelial Cells Activated by Serum Amyloid A

1Department of Rheumatology, University Medical Centre Ljubljana, SI-1000 Ljubljana, Slovenia
2Faculty of Mathematics, Natural Science and Information Technologies, University of Primorska, SI-6000 Koper, Slovenia
3Blood Transfusion Center of Slovenia, Tissue Typing Centre, SI-1000 Ljubljana, Slovenia
4Faculty of Pharmacy, University of Ljubljana, SI-1000 Ljubljana, Slovenia
5Faculty of Medicine, University of Ljubljana, SI-1000 Ljubljana, Slovenia

Correspondence should be addressed to K. Lakota; is.senra.tseug@atokal.ajtak

Received 27 July 2017; Revised 3 November 2017; Accepted 14 November 2017; Published 13 February 2018

Academic Editor: Matteo Piga

Copyright © 2018 K. Lakota et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. RA patients have a higher incidence of cardiovascular diseases compared to the general population. Serum amyloid A (SAA) is an acute-phase protein, upregulated in sera of RA patients. Aim. To determine the effects of medications on SAA-stimulated human coronary artery endothelial cells (HCAEC). Methods. HCAEC were preincubated for 2 h with medications from sterile ampules (dexamethasone, methotrexate, certolizumab pegol, and etanercept), dissolved in medium (captopril) or DMSO (etoricoxib, rosiglitazone, meloxicam, fluvastatin, and diclofenac). Human recombinant apo-SAA was used to stimulate HCAEC at a final 1000 nM concentration for 24 hours. IL-6, IL-8, sVCAM-1, and PAI-1 were measured by ELISA. The number of viable cells was determined colorimetrically. Results. SAA-stimulated levels of released IL-6, IL-8, and sVCAM-1 from HCAEC were significantly attenuated by methotrexate, fluvastatin, and etoricoxib. Both certolizumab pegol and etanercept significantly decreased PAI-1 by an average of 43%. Rosiglitazone significantly inhibited sVCAM-1 by 58%. Conclusion. We observed marked influence of fluvastatin on lowering cytokine production in SAA-activated HCAEC. Methotrexate showed strong beneficial effects for lowering released Il-6, IL-8, and sVCAM-1. Interesting duality was observed for NSAIDs, with meloxicam exhibiting opposite-trend effects from diclofenac and etoricoxib. This represents unique insight into specific responsiveness of inflammatory-driven HCAEC relevant to atherosclerosis.