S-Ibuprofen Effectively Inhibits Thromboxane B2 Levels and Platelet Function in an Experimental Model of Lipopolysaccharide-Stimulated and Non-Stimulated Whole Blood

Abstract

Objective: The present study aimed at testing the effect of S- and R-ibuprofen on thromboxane B₂ (TXB₂), collagen-epinephrine closure time (CEPI-CT) and collagen-adenosine 5′-diphosphate closure time (CADP-CT) in lipopolysaccharide (LPS)-stimulated and non-stimulated human whole blood. Materials and Methods: Whole blood was incubated with S- or R-ibuprofen with and without prior stimulation with LPS. To verify ibuprofen’s potential effects on TXB₂, varying ratios of concentrations of S- and R-ibuprofen ranging from 0 to 100% were used. TXB₂ levels were measured by ELISA. The effects of S- and R-ibuprofen enantiomers on platelet aggregability were tested utilizing a PFA-100 apparatus. Results: In non-stimulated and LPS-stimulated whole blood, S-ibuprofen markedly decreased TXB₂ levels at concentrations ranging from 10 to 200 µg/ml. R-ibuprofen showed its inhibiting effect at concentrations >100 µg/ml. In inflammatory and non-inflammatory conditions, CEPI-CT was prolonged at concentrations of 12.5 and 75 µg/ml for S-ibuprofen and at a concentration of 150 µg/ml of combined R- and S-ibuprofen. S-ibuprofen was significantly more effective than R-ibuprofen (p < 0.05). The combined use of S- and R-ibuprofen did not additively or synergistically prolong CEPI-CTs. CADP-CTs remained unaffected by both enantiomers. Conclusions: S-ibuprofen was more effective than the R-ibuprofen enantiomer in inhibiting TXB₂ plasma levels and aggregability of thrombocytes in non-inflammatory and inflammatory conditions.