Chronic inflammation through foam cells and macrophages is important in atherosclerosis development, and can be considered as therapeutic targets. Cyclooxygenase and NADPH-oxidase were expressed within atherosclerotic lesions. Reactive oxygen species produced by NADPH oxidase were found to trigger the cyclooxygenase-2 expression. The effects of preferential COX-2 inhibitors on ROS produced by Chlamydia-primed human monocytes (THP-1 cells) were evaluated by fluorescence, chemiluminescence, oxymetry, and EPR spin trapping. Fluorescence assays showed an increased production of ROS with Chlamydia versus cells primed by 10(-8)M PMA. COX-2 inhibitors inhibited in a dose-dependent manner the luminol-enhanced CL while ibuprofen and diclofenac increased the chemiluminescence response. By EPR spin trapping, COX-2 inhibitors, ibuprofen, and diclofenac, exhibited a dose-dependent inhibiting effect (10 and 100muM) on the EPR signal appearance. Our cell model combining EPR, chemiluminescence, and oxymetry appeared relevant to study the modulating effects of preferential COX-2 inhibitors on the cell oxidant activity and chronic inflammatory diseases.
|Pages (de - à)||1122-30|
|Nombre de pages||9|
|journal||Biochemical and Biophysical Research Communications|
|Numéro de publication||4|
|Etat de la publication||Publié - 24 déc. 2004|
Contient cette citation
Mouithys-Mickalad, A., Deby-Dupont, G., Dogne, J-M., de Leval, X., Kohnen, S., Navet, R., Sluse, F., Hoebeke, M., Pirotte, B., & Lamy, M. (2004). Effects of COX-2 inhibitors on ROS produced by Chlamydia pneumoniae-primed human promonocytic cells (THP-1). Biochemical and Biophysical Research Communications, 325(4), 1122-30. https://doi.org/10.1016/j.bbrc.2004.10.155