Upregulation of P2Y12 Inhibits Chondrocyte Apoptosis in Lumbar Osteoarthritis Through PI3K/AKT Signaling Pathway

Abstract Lumbar facet osteoarthritis (FJOA) is one of the major causes of severe low back pain and disability worldwide. However, the underlying mechanism of cartilage degeneration in FJOA remains unclear. The purpose of this study was to investigate the expression of P2Y12 in FJOA and its possible role. Changes of chondrocytes in rat facet joints with degenerative changes were observed by HE and ferro red solid green staining. The expression changes of P2Y12, MMP13 and COL2 in FJOA were observed by immunohistochemistry. In vitro, human SW1353 chondrosarcoma cells were stimulated with IL-β to establish chondrocyte apoptosis model. Western blot analysis showed that P2Y12 and cleaved caspase-3 were significantly expressed in SW1353 cells. Co-localization of P2Y12-cleaved Caspase-3 in apoptosis model was detected by double-standard immunofluorescence staining. We demonstrated that P2Y12 may have an anti-apoptotic effect in FJOA chondrocytes apoptosis by inhibiting the expression of P2Y12 by siRNA. In addition, flow cytometry showed that P2Y12 gene knockout enhanced apoptosis induced by P2Y12. Our data suggest that P2Y12 has a chondroprotective effect on FJOA.