| Objective To explore the effect of LncRNA NUTM2A-AS1 on interleukin-1β (IL-1β)-induced chondrocyte damage and its molecular mechanism. Methods Chondrocytes were randomly divided into control group, model group (5 μg/L IL-1β), miR-183-5p+model group, miR-NC+model group, si-LncRNA NUTM2A-AS1+model group, si-TGFα+model group, si-NC+model group, pcDNA-TGFα+si-LncRNA NUTM2A-AS1+model group, pcDNA+si-LncRNA NUTM2A-AS1+model group; real-time fluorescent quantitative PCR (RT-qPCR) was used to detect the expression levels of LncRNA NUTM2A-AS1, miR-183-5p and TGFα mRNA;cell counting kit 8 (CCK-8) was used to detect cell viability; flow cytometry was used to detect chondrocyte apoptosis; enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of TNF-α and IL-6; dual luciferase reporter experiment was used to detect the targeting relationship between NUTM2A-AS1, miR-183-5p, and TGFα. Results In IL-1β-induced chondrocytes, the expressions of LncRNA NUTM2A-AS1 and TGFα were increased, the expression of miR-183-5p was decreased, the activity of chondrocytes was decreased, the apoptosis rate was increased, and the levels of TNF-α and IL-6 were increased. Low expression of LncRNA NUTM2A-AS1, low expression of TGFα or overexpression of miR-183-5p could promote cell proliferation and inhibit apoptosis and inflammatory responses. Conclusions The low expression of LncRNA NUTM2A-AS1 can inhibit IL-1β-induced chondrocyte apoptosis and inflammation by regulating miR-183-5p/TGFα, and promote cell survival. |