THE EFFECT OF IBUPROFEN ON bFGF, VEGF SECRETION AND CELL PROLIFERATION IN THE PRESENCE OF LPS IN HMEC-1 CELLS.

Abstract

Ibuprofen belongs to the group of non-selective cyclooxygenase (COX) inhibitors, also known as traditional non-steroidal anti-inflammatory drugs (NSAIDs). Bacterial lipopolysaccharide, an inflammatory mimicking agent, is responsible for the production of prostaglandins and growth factors (VEGF and bFGF), and as inflammation and angiogenesis are closely associated with osteoarthritis, these factors play a functional role in the cardiovascular system. Therefore, the main aim of our study was to examine the effect of ibuprofen on cell viability and proliferation of HMEC-1 cells and VEGF and bFGF secretion under the inflammatory conditions. The effect of NSAID and LPS on bFGF and VEGF was analyzed by ELISA. Cell viability was measured by the MTT method and the proliferation by the [3H-thymidine test. LPS at 100 µg/mL stimulated the secretion of VEGF and bFGF by HMEC-1 cells. Ibuprofen at concentrations of 0.1 and 1 mM intensified the secretion of LPS-induced VEGF in a statistically significant manner (p < 0.05). Both concentrations of ibuprofen inhibited LPS-stimulated bFGF secretion (p < 0.05) in HMEC-1 in a concentration-dependent manner. The non-selective COX inhibitor decreased proliferation and cell viability induced by LPS in a concentration-dependent manner. The observed effects of ibuprofen on endothelial cells may further explain its effects as well as other NSAIDs on the cardiovascular system function in cardiovascular diseases.