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

Abstract

Interleukin (IL)1induced chondrocyte apoptosis is associated with the pathogenesis of arthritis. Plateletrich 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 IL1induced 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 kit8 assay, cell apoptosis was evaluated by flow cytometry, and the expression of apoptosis, anabolism and catabolismassociated 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 IL1 induced cell apoptosis. Treatment with PRP significantly attenuated cell apoptosis in IL1treated chondrocytes, and altered apoptosisassociated expression at the gene and protein level. Furthermore, treatment with PRP significantly reduced matrix metalloproteinase production and promoted anabolism of cartilage extracellular matrix under IL1 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.