Carboxymethyl‑chitosan attenuates inducible nitric oxide synthase and promotes interleukin‑10 production in rat chondrocytes
- Ying Kong
- Yuanmin Zhang
- Xiaowei Zhao
- Guodong Wang
- Qingkuan Liu
Published online on: October 3, 2017
Osteoarthritis (OA) is a common age‑related degenerative joint disease, which is caused by the breakdown of joint cartilage and the underlying bone. Carboxymethyl (CM)‑chitosan is a soluble derivative of chitosan that has similar physicochemical properties to the extracellular proteoglycans identified in hyaline cartilage. Previous studies have demonstrated that CM‑chitosan serves a protective role in a rabbit OA model. The aim of the present study was to investigate the effect of CM‑chitosan on NO production and inflammation through its upregulation of interleukin (IL)‑10, and the activation of the janus kinase (JAK)/signal transducer and activator of transcription (STAT)/suppressor of cytokine signaling (SOCS) signaling pathway. In the present study primary rat chondrocytes were induced to inflammation with 2 µg/ml lipopolysaccharide. The cells were subsequently subjected to increasing concentrations of CM‑chitosan (50, 100 and 200 µg/ml) and the relative mRNA and protein expression of inducible nitric oxide synthase (iNOS), IL‑10, JAK1, STAT3 and SOCS3 were measured by RT‑qPCR and western blot analysis respectively. The results revealed that CM‑chitosan attenuated inflammation by significantly reducing iNOS expression and upregulating the anti‑inflammatory cytokine IL‑10 in a dose‑dependent manner (P<0.05). The expression of JAK1, STAT3 and SOCS3 were also significantly upregulated by CM‑chitosan (all P<0.05). The protective role of CM‑chitosan against NO production was due to its upregulation of IL‑10 and its activation of the JAK/STAT/SOCS signaling pathway.