lncRNA-NR024118 overexpression reverses LPS-induced inflammatory injury and apoptosis via NF-κB/Nrf2 signaling in ATDC5 chondrocytes

摘要

Osteoarthritis (OA) is one of the most prevalent types of chronic joint diseases. Chondrocytes survival is closely associated with the destruction of joints in patients with OA. Long noncoding RNAs (lncRNAs) serve a critical role in OA. However, to the best of our knowledge, the role of lncRNAs NR024118 in OA has not been examined. In the present study, the expression levels of NR024118 in lipopolysaccharide (LPS)-induced chondrocytes was measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and the apoptosis levels of cells was determined using flow cytometry. The levels of scavenged reactive oxygen species and expression levels of the antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), and heme oxygenase-1 (HO-1) were measured using specialized detection kits. The expression of interleukin (IL)-1β, IL-6 and IL-18 were measured using ELISA. Expression of the cell apoptosis markers Bcl-2, Bax, Bcl-2-like protein 11, NF-κB, phosphorylated (p)-NF-κB inhibitor β (IκBβ), IκBβ, p-transcription factor p65 (p65) and p65, and nuclear factor erythroid-2 related factor 2 (Nrf2) signaling pathways-associated proteins, Nrf2, HO-1 and quinone oxidoreductase-1 were detected by western blot analysis and RT-qPCR. The results indicated that in ATDC5 cells, apoptosis, oxidative stress and inflammation were significantly increased and the expression level of NR024118 was significantly decreased by LPS-mediated induction. NR024118 overexpression significantly reversed the effects of LPS treatment in the ATDC5 cell line. In addition, the overexpression of NR024118 decreased NF-κB expression levels and activated the Nrf2 signaling pathways in LPS-induced ATDC5 cells. The present study demonstrated that NR024118 attenuated the effects of LPS-induction on ATDC5 cells. These results suggest that NR024118 may be a potential target for diagnosis and treatment of OA.