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

Chondrocyte Apoptosis is important in pathogenesis of osteoarthritis. Chitosan is a non-toxic, biodegradable and biocompatible glycosaminoglycan. 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-1beta (IL-1beta). After treatment with various concentrations of CM-chitosan (50, 100, 200 microg/ml), the apoptotic rate, mitochondrial function, nitric oxide production, and the levels of inducible nitric oxide synthase (iNOS) mRNA and Reactive Oxygen Species in IL-1beta-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 iNOS mRNA expression, and scavenge Reactive Oxygen Species in chondrocytes induced by IL-1beta. The results suggested that the inhibitory effects of CM-chitosan on IL-1beta-induced chondrocyte Apoptosis were possibly due to the protection of mitochondrial function, the decline in the levels of nitric oxide and Reactive Oxygen Species.