Sodium nitroprusside induces apoptosis of rabbit chondrocytes

摘要

Osteoarthritis (OA) is characterized by a slowly progressing degradation of the matrix and destruction of articular cartilage. Apoptosis of chondrocyte is accounted for the mechanism of OA. Nitric oxide (NO), as a stimulus, has been shown to induce chondrocyte apoptosis by activating the matrix metalloproteinases (MMPs), increasing the expression of cyclooxygenase 2 (COX-2) and the level of prostaglandin E_2 (PGE_2), inhibiting the proteoglycan synthesis and type Ⅱ collagen expression. In this study, sodium nitroprusside (SNP) was administered to be the NO donor to explore the mechanism of NO-induced apoptosis of rabbit chondrocytes obtained from six weeks old New Zealand rabbits. CCK-8 assay revealed the inhibitory effect of SNP on cell viability. We used flow cytometry (FCM) to assess the form of cell death by Annexin-Ⅴ/propidium iodide (PI) double staining, and evaluate the change of mitochondria] membrane potential (△Ψm). We found that the SNP induced chondrocyte apoptosis in a dose- and time-dependent manner and an observable reduction of △Ψ_m In conclusion, our findings indicate that SNP induces apoptosis of rabbit chondrocytes via a mitochondria-mediated pathway.