Carboxymethyl-chitosan protects rabbit chondrocytes from interleukin-1β-induced apoptosis

Chondrocyte apoptosis is important in pathogenesis of osteoarthritis. Chitosan is a non-toxic, biodegradable and biocompatible glycosammoglycan. In this study, the effects of carboxymethyl-chitosan (CM-chitosan), a soluble derivative of chitosan, on chondrocyte apoptosis were investigated. Primary rabbit chondrocytes were cultured and induced to apoptosis by 10 ng/ml interleukin-1 After treatment with various concentrations of CM-chitosan (50, 100, 200 mu g/ml), the apoptotic rate, mitochondrial function, nitric oxide production, and the levels of inducible nitric oxide synthase (NOS) mRNA and reactive oxygen species in IL-1 beta-induced chondrocytes were examined. The results showed that CM-chitosan could inhibit chondrocyte apoptosis in a dose-dependent manner. Furthermore, it could partly restore the levels of mitochondrial membrane potential and ATP, decrease nitric oxide production by down-regulation of NOS mRNA expression, and scavenge reactive oxygen species in chondrocytes induced by IL-1 beta. The results suggested that the inhibitory, effects of CM-chitosan on IL-1 beta-induced chondrocyte apoptosis were possibly due to the protection of mitochondrial function, the decline in the levels of nitric oxide and reactive oxygen species. (c) 2006 Elsevier B.V All rights reserved.