In vitro inhibition of IL-1beta catabolic effects on cartilage: a mechanism involved on diacerein anti-OA properties.
Fiche publication
Date publication
janvier 2008
Journal
Biorheology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr DE ISLA Natalia
Tous les auteurs :
de Isla NG, Stoltz JF
Lien Pubmed
Résumé
Osteoarthritis (OA) is a progressive joint disease which represents a combination of several disorders leading to cartilage degradation. The main characteristic of OA is an imbalance between chondrocyte anabolic and catabolic activities. Cytokines produced by the synovium and chondrocytes, especially interleukin 1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha), play a significant role in the degradation of cartilage. They stimulate the production of nitric oxide (NO), which is involved in cartilage catabolism and also may induce the apoptosis of chondrocytes. The IL-1beta produced in activated chondrocytes or synovium may modulate disease progression in OA and should therefore be considered a potential target for therapeutic interventions. Drug and non-drug treatments are used to relieve pain and/or swelling in OA. Diacerein is a slow-acting drug that may slow down the breakdown of cartilage and relieve pain and swelling. It is not clear whether diacerein works but it has been proposed that diacerein acts as a symptom-modifying and perhaps disease-structure modifying drug.
Mots clés
Animals, Anthraquinones, pharmacology, Anti-Inflammatory Agents, pharmacology, Apoptosis, drug effects, Cartilage, drug effects, Cartilage, Articular, cytology, Cells, Cultured, Chondrocytes, drug effects, Glycosaminoglycans, metabolism, Interleukin-1beta, antagonists & inhibitors, Nitric Oxide, metabolism, Osteoarthritis, drug therapy, Rats, Synovial Membrane, drug effects, Tumor Necrosis Factor-alpha, drug effects
Référence
Biorheology. 2008 ;45(3-4):433-8