Platelet-rich plasma inhibits inflammation, apoptosis, and the NLRP3/Caspase-1 pathway and induces matrix metalloproteinases and proliferation of IL-1β-induced articular chondrocytes by downregulating T-box transcription factor 3

Objectives Osteoarthritis (OA) is a chronic joint disease characterized by osteoproliferation and the degeneration destruction of articular cartilage. Platelet-rich plasma (PRP) rich in various growth factors that have been reported to promote bone defect repair. This study examined specific role mechanism PRP OA. Methods OA model cells were created treating chondrocytes with IL-1β. After treatment or/and T-box transcription factor 3 (TBX3)-overexpression plasmid, TBX3 expression was monitored via RT-qPCR, western blotting, immunofluorescence assays. IL-1β, IL-33, Caspase-3 levels detected ELISA kits. Levels NLRP3, Caspase-1, MMP9, MMP13, COL2A1 evaluated cell proliferation assessed CCK-8 assay. Results Our results showed upregulated IL-1β-induced chondrocytes. IL-1β stimulation induced inflammation production matrix metalloproteinases, activated NLRP3/Caspase-1 pathway, inhibited chondrocytes; however, all those affects mediated could be markedly reversed PRP. We also found alleviated inflammation, apoptosis, extracellular degradation inhibiting TBX3. findings suggest alleviates progression vitro downregulating Conclusion suppressed TBX3, which may its action