2024, Vol. 28 ›› Issue (32): 5167-5171

Platelet-rich fibrin regulates apoptosis to promote cartilage repair in rats with knee osteoarthritis

Hou Zengtao1, Dong Zhiwei1, Zhang Jinfeng1, Yang Xiaohui2, Fan Xiao2   

Abstract: BACKGROUND: Platelet-rich fibrin (PRF) is a second generation platelet concentrate with the advantages of simple operation, no anticoagulant, and high bioactivity, which has been applied in the fields of trauma repair, bone defect repair, and tendon soft tissue repair, and has been proved to have a certain tissue repair-promoting effect.
OBJECTIVE: To study the repair effect of PRF on articular cartilage tissue in rats with knee osteoarthritis.
METHODS: Thirty-six Sprague-Dawley rats were randomly divided into normal group, model group, and PRF group, with 12 rats in each group. Rats in the normal group did not undergo any treatment. In the model group, animal models of knee osteoarthritis were prepared and rat models were then given physiological saline into the joint cavity once a week after surgery. Rat models of knee osteoarthritis were also prepared in the PRF group, and autologous PRF was injected into the joint cavity once a week after surgery. After 5 weeks of continuous treatment, tissue samples were taken. Hematoxylin-eosin staining was used to observe the morphology of cartilage tissue. Tunel staining was used to detect chondrocyte apoptosis, ELISA was used to detect inflammatory factor levels. Western blot and RT-PCR were used to detect Bcl-2, Bax, and Caspase-3 expression in protein and mRNA levels, respectively.
RESULTS AND CONCLUSION: The model group had severe cartilage tissue damage, while the PRF group had significantly improved cartilage tissue morphology compared with the model group. The model group had more apoptotic chondrocytes. Compared with the model group, the mean absorbance of Tunel positive staining in the PRF group significantly decreased (P < 0.01). The levels of interleukin-1β, interleukin-6 and tumor necrosis factor-α were significantly increased in the model group and PRF group compared with the normal group (P < 0.01) and were significantly decreased in the PRF group compared with the model group (P < 0.01). The relative expressions of Bax and Caspase-3 at protein and mRNA levels were significantly increased in the model group and PRF group compared with the normal group (P < 0.01), while the relative expressions of Bcl-2 at protein and mRNA were significantly decreased (P < 0.01). Compared with the model group, the relative expression of Bax and Caspase-3 at protein and mRNA levels were significantly decreased in the PRF group (P < 0.01), while the relative expressions of Bcl-2 at protein and mRNA levels were significantly increased (P < 0.01). To conclude, PRF can inhibit chondrocyte apoptosis by inhibiting the expression of pro-inflammatory factors, thereby promoting cartilage tissue repair in knee osteoarthritis rats.

Key words: knee osteoarthritis, platelet-rich fibrin, inflammation, apoptosis, platelet concentrate