Chondrocyte apoptosis induced by nitric oxide.

摘要: Chondrocytes stimulated with IL-1 produce high levels of nitric oxide (NO), which inhibits proliferation induced by transforming growth factor-beta or serum. This study analyzes the role NO and in induction chondrocyte cell death. generated from sodium nitroprusside apoptosis cultured chondrocytes as demonstrated electron microscopy, 4',6-dianidino-2-phenylindole dihydrochloride staining, FACS analysis, histochemical detection DNA fragmentation. Similar results were obtained two other donors, 3-morpholinosynonimide-hydrochloride s-nitroso-N-acetyl-D-L-penicillamine. In contrast, oxygen radicals hypoxanthine/xanthine oxidase caused necrosis but did not induce apoptosis. To analyze whether endogenously induces apoptosis, IL-1, there was no evidence for apoptotic changes. Combinations inducers such lipopolysaccharide, tumor factor, interferon-gamma also failed to trigger IL-1-stimulated are known that react form products can death systems. We thus tested combination radical scavengers N-acetyl cysteine, dimethyl sulfoxide, 5,5'-dimetylpyrroline 1-oxide. Under these conditions able inhibited a dose-dependent manner synthase inhibitor N-monomethyl L-arginine. Conversely, endogenous inflammatory mediators under simultaneous production reduced. These suggest NO, radicals, is primary inducer human articular chondrocytes.