Ibuprofen inhibits adhesiveness of monocytes to endothelium and reduces cellular oxidative stress in smokers and non-smokers

Background Cigarette smoking is a major risk factor in atherosclerosis and a useful model from which to study chronic inflammation. We compared monocy te function, lipid profiles and inflammatory markers in smokers and non-smo kers, before and after oral ibuprofen intake. The adhesion of freshly isola ted monocytes to native and tumour necrosis factor a (TNFa) stimulated huma n umbilical vein endothelial cells (HUVEC), as well as superoxide anion (O- 2(-)) levels and hydrogen peroxide (H2O2) production in resting and phorbol myristate acetate (PMA) stimulated monocytes were determined. Materials and methods A group of nine smokers without any other coronary ri sk factor was compared with an age-matched group of 9 non-smokers. Tests we re performed before and after a two-week course of oral ibuprofen (600 mg d ay(-1)). Results In smokers before ibuprofen, monocyte adhesion to native and TNFa-s timulated HUVEC was increased (P < 0001 and P < 0.01, respectively), and so were O-2(-) levels in native and PMA-stimulated monocytes (P < 0.01 and P < 0.001, respectively). Ibuprofen reduced the adhesion of monocytes to nati ve and stimulated HUVEC (P < 0.001) and O-2(-) generation by resting and PM A-stimulated cells (P < 0.01) in both groups. H2O2 production by resting an d PMA-stimulated monocytes was reduced in smokers and non-smokers (P < 0.01 ). Interestingly, ibuprofen increased HDL cholesterol levels in smokers (P < 0.01) and non-smokers (P < 0.001), and reduced the level of triglycerides in smokers (P < 0.05). Conclusion Oral administration of ibuprofen reduced the adhesion of monocyt es to HUVEC, suppressed oxidative stress and increased HDL cholesterol leve ls in smokers and non-smokers.