OBJECTIVE: To evaluate the degree of lipid peroxidation of synoviocytes from patients with rheumatoid arthritis (RA), osteoarthitis (OA), and controls and to look at the production of nitric oxide (NO) and its involvement in this process. METHODS: Human synoviocytes were isolated from synovial tissues from patients with RA, OA, and from healthy controls. Cells were maintained in culture for up to 3 culture passages. Lipid peroxidation, verified by the production of malonaldehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE), was determined by colorimetric assay. NO was evaluated by estimating the stable NO metabolite nitrite by the Griess method in the supernatants of unstimulated and interleukin (IL)-1beta and tumor necrosis factor (TNF)-a stimulated cells. RESULTS: Increased levels of lipid peroxidation were observed for OA-derived synoviocytes compared to RA and controls. The cells in each experimental group produced low amounts of NO both in basal and in stimulated conditions. CONCLUSION: In OA, synovial cells underwent a lipid peroxidation process that did not occur in synoviocytes from RA or controls even in the absence of a detectable production of the reactive nitrogen intermediate NO. We can postulate that this peroxidation process might be due to the action of NO secreted by chondrocytes that are known to produce higher levels of this radical in OA compared to RA.
OBJECTIVE: To evaluate the degree of lipid peroxidation of synoviocytes from patients with rheumatoid arthritis (RA), osteoarthitis (OA), and controls and to look at the production of nitric oxide (NO) and its involvement in this process. METHODS:Human synoviocytes were isolated from synovial tissues from patients with RA, OA, and from healthy controls. Cells were maintained in culture for up to 3 culture passages. Lipid peroxidation, verified by the production of malonaldehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE), was determined by colorimetric assay. NO was evaluated by estimating the stable NO metabolite nitrite by the Griess method in the supernatants of unstimulated and interleukin (IL)-1beta and tumor necrosis factor (TNF)-a stimulated cells. RESULTS: Increased levels of lipid peroxidation were observed for OA-derived synoviocytes compared to RA and controls. The cells in each experimental group produced low amounts of NO both in basal and in stimulated conditions. CONCLUSION: In OA, synovial cells underwent a lipid peroxidation process that did not occur in synoviocytes from RA or controls even in the absence of a detectable production of the reactive nitrogen intermediate NO. We can postulate that this peroxidation process might be due to the action of NO secreted by chondrocytes that are known to produce higher levels of this radical in OA compared to RA.
Authors: Qin Shi; France Vaillancourt; Véronique Côté; Hassan Fahmi; Patrick Lavigne; Hassan Afif; John A Di Battista; Julio C Fernandes; Mohamed Benderdour Journal: Arthritis Res Ther Date: 2006 Impact factor: 5.156
Authors: Alexander Franz; Laura Joseph; Constantin Mayer; Jan-Frieder Harmsen; Holger Schrumpf; Julia Fröbel; Martin S Ostapczuk; Rüdiger Krauspe; Christoph Zilkens Journal: Orthop Rev (Pavia) Date: 2018-06-14