Abstract
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.
Original language | English |
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Pages (from-to) | 1122-30 |
Number of pages | 9 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 325 |
Issue number | 4 |
DOIs | |
Publication status | Published - 24 Dec 2004 |
Keywords
- Arteriosclerosis
- Cell Differentiation
- Cell Line
- Chlamydophila pneumoniae
- Cyclooxygenase Inhibitors
- Dose-Response Relationship, Drug
- Free Radicals
- Humans
- Inflammation
- Macrophages
- Monocytes
- Reactive Oxygen Species
- Tetradecanoylphorbol Acetate