LAUSR

Objective: Platelet‐rich plasma (PRP) has been reported to alleviate degenerative pathological damage to joint cartilage. This study aimed to investigate the effect of PRP on Wnt/&bgr;‐catenin signaling in rabbit chondrocytes. Methods: Using 3‐month‐old New Zealand white rabbits, PRP was prepared from venous blood, and chondrocytes were cultured from knee joint cartilage and identified by staining for type II collagen and proteoglycan. The effects of PRP on chondrocyte viability were measured. The chondrocytes were divided into 5 groups: control, IL‐1&bgr;, PRP (100‐fold dilution), Dkk‐1 (100 ng/mL) and Dkk‐1 + PRP. The IL‐1&bgr;, PRP, Dkk‐1 and Dkk‐1 + PRP groups were treated with interleukin (IL)‐1&bgr; (50 &mgr;L, 10 &mgr;g/mL) for24 h. Chondrocyte morphology was observed by electron microscopy. Levels of carboxy terminal peptide (CTX‐II) and cartilage oligomeric matrix protein (COMP) in culture media were measured by ELISA. Wnt‐1, &bgr;‐catenin and GSK‐3&bgr; mRNA and protein expression were determined by RT‐PCR and western blot respectively. Results: PRP enhanced chondrocyte proliferation. Chondrocytes in the IL‐1&bgr; group showed ultrastructural abnormalities that were less pronounced in the PRP, Dkk‐1 and Dkk‐1 + PRP groups. CTX‐II and COMP concentrations were higher in the IL‐1&bgr; group than in the control, PRP, Dkk‐1 and Dkk‐1 + PRP groups (P < 0.05). The IL‐1&bgr; group had higher mRNA and protein Wnt1 and &bgr;‐catenin levels and lower GSK‐3&bgr; levels than the control, PRP, Dkk‐1 and Dkk‐1 + PRP groups (P < 0.05). Conclusion: PRP may protect chondrocytes activated by IL‐1&bgr; via inhibiting Wnt/&bgr;‐catenin signaling. HighlightsPlatelet‐rich plasma enhanced chondrocyte proliferation.PRP alleviated the ultrastructural damage of chondrocytesPRP reduces the contents of CTX‐II and COMP in chondrocytes culture mediumPRP protect chondrocytes activated by IL‐1&bgr; via inhibiting Wnt/&bgr;‐catenin signaling