Lysyl oxidase inhibits TNF-α induced rat nucleus pulposus cell apoptosis via regulating Fas/FasL pathway and the p53 pathways.

AIMS Intervertebral disc degeneration (IVDD) has been regarded as the main cause of low back pain, which affects 80% of adults and still lack effective treatment. In IVDD, nucleus pulposus (NP) cell apoptosis has widely existed. Lysyl oxidase (LOX) has been demonstrated to protect chondrocyte against apoptosis in the TNF-α-treated human chondrocytes. Therefore, in this study, we investigated the anti-apoptosis effect of LOX on TNF-α-treated rat NP cells. MAIN METHODS Real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and western blot analyses were used to detect the expression of LOX in TNF-α-treated rat NP cells. Then, the toxicity of exogenous LOX and its protective effect was evaluated by Cell Counting kit-8 (CCK-8). NP cell apoptosis was evaluated by flow cytometry analysis and TUNEL assay. The regulatory effects of LOX on the expression of extracellular matrix (ECM) molecules in TNF-α-treated rat NP cells were measured by RT-qPCR, western blot, and ELISA analyses. The molecular mechanism of LOX in regulating NP cell apoptosis was investigated by RT-qPCR and western blot analyses. KEY FINDINGS The expression of LOX in TNF-α-treated rat NP cells was significantly decreased. Exogenous LOX preserved the cell viability, reduced the rate of apoptosis and improved the ECM secretion in TNF-α-treated rat NP cells. Further molecular mechanism investigation showed that LOX inhibited the Fas/FasL and p53 pathways. SIGNIFICANCES LOX played an anti-apoptotic role in TNF-α-treated rat NP cells which could be a promising reagent in IVDD treatment.