LAUSR

We aimed to investigate the role of oxidized low density lipoprotein (ox-LDL) in tumor necrosis factor-α (TNF-α) mediated chondrocyte death and explore the mechanisms. Ten osteoarthritis (OA) and normal control cartilage tissue and synovial fluid (SF) samples were collected, and the expression of lectin-like ox-LDL receptor-1 (LOX-1) and ox-LDL level was examined by real time quantitative PCR and enzyme-linked immunosorbent assay (ELISA). An in vitro chondrocyte model was established by the introduction of TNF-α and ox-LDL, cell death was analyzed by trypan blue assay and the mechanisms were explored based on the apoptosis related pathway and autophagy pathway. Significantly increased ox-LDL level (70.30±17.83 vs. 37.22±19.97, P<0.05) in SF sample and LOX-1 expression level (0.51±0.10 vs. 0.32±0.04, P<0.05) in cartilage tissue was found in OA patients compared to those corresponding samples from control subjects. Ox-LDL could facilitate TNF-α mediated chondrocyte death and this effect could be blocked by LOX-1 antibody neutralization. Autophagy inhibition by 3-MA and Atg-5 siRNA could reverse the cell death effect mediated by TNF-α and ox-LDL co-treatment on chondrocytes. Oxidized low density lipoprotein facilitates tumor necrosis factor-α mediated chondrocyte death via its interaction with LOX-1, and autophagy is involved in the mechanisms.