100 Section - Platelet-Rich Plasma Attenuates Chondrocyte Senescence and Knee Osteoarthritis Progression

Knee osteoarthritis (KOA) is a common degenerative disease characterized by cartilage degradation and damage. Chondrocyte senescence plays a key role in disease progression, with the accumulation of senescent cells disrupting cellular function and exacerbating cartilage damage. Platelet-rich plasma (PRP), rich in growth factors, promotes tissue repair and regeneration. It remains unclear whether PRP regulates the progression of KOA by modulating cellular senescence.

To evaluate the effects of PRP on chondrocyte senescence in KOA and investigate its potential underlying mechanisms.

Design:

Chondrocyte cell cycle, senescence markers, SASP secretion, and extracellular matrix (ECM) integrity were evaluated by Western blot, RT-qPCR, flow cytometry, immunofluorescence, and β-galactosidase staining. Mitochondrial function and antioxidative properties were assessed by measuring mitochondrial membrane potential and ROS levels. Additionally, a rat KOA model was established by anterior cruciate ligament transection (ACLT), followed by weekly intra-articular injections of PRP or PBS for four weeks. Knee joint samples were collected at 8 and 12 weeks post-surgery for gross morphology, imaging, and histological analysis.

Results:

In vitro experiments revealed that PRP inhibited chondrocyte senescence and ECM degeneration, as evidenced by increased expression of COL2A1 and ACAN, and decreased expression of MMP13, ADAMTS5, P16, P21, and P53. Additionally, mRNA expression of SASP (Il1b, Il6, and Tnf) and SA-β-gal positivity were suppressed. Furthermore, PRP was found to modulate cell cycle arrest, improve mitochondrial function, and enhance antioxidative properties. In vivo experiments demonstrated that intra-articular PRP injection repaired damaged articular cartilage, reduced OARSI scores, improved trabecular bone parameters, and upregulated the expression of COL2A1 and ACAN, while suppressing the expression of senescence-related proteins P16, P21, and P53 in the cartilage of the KOA model.

Conclusion:

Our results demonstrated that PRP alleviates OA progression by inhibiting chondrocyte senescence.