Calcitonin protects rat chondrocytes from IL‑1β injury via the Wnt/β‑catenin pathway
- Mingxiao Bai
- Lei Ge
- Hui Chen
- Qunhua Jin
Published online on: July 24, 2019
Copyright: © Bai et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
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The present study investigated whether the Wnt/β‑catenin pathway was involved in the protective effect of calcitonin (CT) in interleukin‑1β (IL‑1β)‑injured rat chondrocytes. Chondrocytes were acquired from the articular cartilage of 4‑week‑old rats and treated with 10 ng/ml IL‑1β to stimulate an in vitro osteoarthritis model. CT (10 and 50 nM) and 5 µm IWR‑1‑endo (a Wnt/β‑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‑1β 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 β‑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/β‑catenin pathway to exert a protective effect on IL‑1β‑injured rat chondrocytes.