Long-term NSAID treatment directly decreases COX-2 and mPGES-1 production in the articular cartilage of patients with osteoarthritis

摘要: Summary Objective To simultaneously study the effect of a selective cyclooxygenase-2 (COX-2) inhibitor and that classic non-steroidal anti-inflammatory drug (NSAID) on expression pro-inflammatory genes in cartilage patients with severe knee osteoarthritis (OA) cultured human OA chondrocytes. Methods A 3-month clinical trial was carried out 30 scheduled for replacement surgery. Patients were randomized into two groups: treated celecoxib (CBX) aceclofenac (ACF). who did not want to be served as control group. After surgery, processed molecular biology studies. We also employed chondrocytes from different examine NSAID effects gene cells stimulated interleukin (IL)-1β. Results Both CBX ACF inhibited COX-2, microsomal prostaglandin E synthase-1 (mPGES-1) inducible nitric oxide synthase (iNOS) synthesis articular patients. In chondrocytes, both decreased COX-2 mPGES-1 E2 (PGE2) release induced by IL-1β, while no observed or iNOS synthesis. patients, only tumor necrosis factor alpha IL-1β cartilage, diminished cytokine Conclusions PGE2 decrease These data suggest prolonged therapy blocking agents decreases production direct inhibition activity, but down-regulating cartilage. However, seem have profile controlling