[Death of articular chondrocytes. Mechanisms and protection].
APOPTOSIS IN JOINT CARTILAGE: Apoptosis is the physiologically programmed death of cells to be distinguished from necrosis which caused non-programmed cell death. In joint cartilage, more than 50% of the chondrocytes show signs of apoptosis compared with 10% in normal cartilage. ROLE OF NITRIC OXIDE: In osteoarthritis the production of nitric oxide (NO) appears to be increased, inducing apoptosis of articular chondrocytes stimulated by interleukin 1. NO inhibitors can limit the progression of experimentally induced joint lesions in animal models. IN VITRO RESULTS: The protective effect of the chondroitin sulfates CS4 and CS6 against death of chondrocytes exposed to NO has been demonstrated in vitro. Chondrocytes for New Zealand white rabbits were cultivated in the presence of an NO donor for exposure durations from 12 to 72 hours, with or without adding CS 4&6 to the culture medium. After 3 days of culture, NO induced a significant rise in the number of apoptotic chondrocytes. In 70% of the cases, preventive treatment with 100 micrograms/ml CS 4&6 lowered the number of dead cells. This cytoprotective effect reached a mean 28% and was inversely dependent on the duration of exposure to the NO donor.
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Service de Rhumatologie, Centre hospitalier Lyon-Sud, Pierre-Bénite.
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D002809:Chondroitin Sulfates / Q000494:pharmacology / Q000502:physiology; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology; D010003:Osteoarthritis / Q000473:pathology / Q000503:physiopathology*; D011817:Rabbits
D009569:Nitric Oxide; D002809:Chondroitin Sulfates
La mort des chondrocytes articulaires. Mécanisme et protection.