Platelet-rich plasma contributes to chondroprotection by repairing mitochondrial function via AMPK/NF-κB signaling in osteoarthritic chondrocytes

Osteoarthritis (OA), also known as degenerative osteoarthritis, has a complex etiology, and its pathogenesis remains unclear. Platelet-rich plasma (PRP) therapy has been widely used in medicine and other related professions since its clinical application was first reported in the 1980 s and the 1990 s. This study aimed to investigate the effects and potential mechanisms of PRP in OA. An in vitro model of osteoarthritis was constructed by lipopolysaccharide (LPS) stimulation, and the effect of PRP on LPS-induced chondrocytes was evaluated. The results indicated that although LPS inhibited chondrocyte proliferation and promoted inflammation and apoptosis, these effects were reversed by PRP. In addition, the LPS-suppressed expression of aggrecan, TGF-β, PDGF, and COL2A1 was restored by PRP, whereas the LPS-enhanced expression of MMP3 was suppressed by PRP. Furthermore, PRP inhibited LPS-induced mitochondrial damage by suppressing reactive oxygen species production, mitochondrial permeability transition pore opening, Drp1 expression, and upregulating Mfn1 expression. In addition, PRP inhibited the phosphorylation of AMPK and NF-κB. Collectively, this study indicates that PRP might be a potential therapeutic candidate for the treatment of OA by repairing mitochondrial function through the activation of AMPK/NF-κB signaling.