Calcitonin protects rat chondrocytes from IL-1β injury via the Wnt/β-catenin pathway

The present study investigated whether the Wnt/beta-catenin pathway was involved in the protective effect of calcitonin (CT) in interleukin-1 beta (IL-1 beta)-injured rat chondrocytes. Chondrocytes were acquired from the articular cartilage of 4-week-old rats and treated with 10 ng/ml IL-1 beta to stimulate an in vitro osteoarthritis model. CT (10 and 50 nM) and 5 mu m IWR-1-endo (a Wnt/beta-catenin inhibitor) was used for treatment. The proliferation and apoptosis of rat articular chondrocytes were measured using a cell counting kit-8 assay and Annexin V/PI staining, respectively. Expression of matrix-metalloproteinases (MMP)-13 MMP3 and MMP9 and aggrecanases [metalloproteinase thrombospondin motifs (ADAMTS4 and ADAMTS5)] were measured to assess the degradation of the cartilage extracellular matrix. The results of the present study demonstrate that CT protected rat chondrocytes from IL-1 beta stimulation by enhancing cell viability, suppressing apoptosis and decreasing the expression of matrix metallopeptidase (MMP) MMP13, MMP3, MMP9, ADAMTS4 and ADAMTS5. CT treatment also upregulated dickkopf-1 and downregulated beta-catenin. IWR-1-endo demonstrated similar effects to that of CT treatment. The administration of CT in addition to IWR-1-endo reinforced the change trends induced by CT or IWR-1-endo in the aforementioned events, indicating that CT possibly acted via the Wnt/beta-catenin pathway to exert a protective effect on IL-1 beta-injured rat chondrocytes.