IL-1 beta induces the degradation of equine articular cartilage by a mechanism that is not mediated by nitric oxide.

Proteoglycan degradation was induced in young equine articular cartilage explants cultured for eight days in the presence of 50 ng/ml recombinant human interleukin-1 beta. Degradation was initiated after 6 hours of exposure to the cytokine. This was accompanied by an induction of nitric oxide synthesis and a decrease in the incorporation of [36S]sulphate into the glycosaminoglycan chains of proteoglycans. The addition of 1mM N-iminoethyl-L-ornithine (an inhibitor of nitric oxide synthase) to the explant cultures in the presence of rhIL-1 beta suppressed the synthesis of NO and restored proteoglycan synthesis to control levels. However, treatment of explants with LNIO did not overcome proteoglycan degradation. These results indicate that although IL1 beta regulates both proteoglycan synthesis and degradation in equine cartilage explants, only the inhibition of proteoglycan synthesis is mediated by nitric oxide.