Platelet-rich plasma protects rat chondrocytes from interleukin-1β-induced apoptosis

Interleukin (IL)-1 beta-induced chondrocyte apoptosis is associated with the pathogenesis of arthritis. Platelet-rich plasma (PRP), which is derived from the patient's own blood and contains numerous growth factors, has the potential for arthritis treatment. Therefore, the present study aimed to determine the effects of PRP on chondrocyte apoptosis, under IL-1 beta-induced pathological conditions. Chondrocytes isolated from the knee joint of Sprague Dawley rats were used in the present study. Cell viability was determined using the Cell Counting kit-8 assay, cell apoptosis was evaluated by flow cytometry, and the expression of apoptosis-, anabolism-and catabolism-associated genes were detected by quantitative polymerase chain reaction; protein expression was detected by western blot analysis. The results demonstrated that 10% PRP in the culture medium increased chondrocyte proliferation, whereas IL-1 beta induced cell apoptosis. Treatment with PRP significantly attenuated cell apoptosis in IL-1 beta-treated chondrocytes, and altered apoptosis-associated expression at the gene and protein level. Furthermore, treatment with PRP significantly reduced matrix metalloproteinase production and promoted anabolism of cartilage extracellular matrix under IL-1 beta treatment. The present study demonstrated the protective effects of PRP on chondrocyte apoptosis and extracellular matrix anabolism, and provided scientific evidence to support the potential use of PRP as a promising therapeutic strategy for the treatment of arthritis.