Abstract
Osteoarthritis (OA) is a common age‑related joint disorder, for which no effective disease‑modifying drugs are currently available. Long non‑coding RNAs (lncRNAs) are involved in the occurrence of OA. lncRNA small nucleolar RNA host gene 16 (SNHG16) has been reported to regulate inflammation; however, the exact biological function of SNHG16 in OA and its underlying mechanism of action remain unclear. In this study, gene and protein expression levels were detected using reverse transcription‑quantitative PCR and western blotting, respectively. Cell apoptosis was analyzed using flow cytometry and ELISA was performed to detect TNF‑α levels. The interactions between lncRNA SNHG16 and microRNA (miR)‑373‑3p were examined using the dual‑luciferase reporter assay. lncRNA SNHG16 was upregulated in OA tissue compared with normal joint tissue. The expression levels of collagen II were significantly reduced in OA tissue compared with normal tissue. Similarly, aggrecan expression levels were significantly reduced in IL‑1β‑treated CHON‑001 cells compared with the controls. In addition, the protein expression levels of MMP13 were significantly increased in OA tissues and IL‑1β‑treated CHON‑001 cells compared with the controls. SNHG16 knockdown significantly increased the expression levels of aggrecan, and decreased the expression levels of MMP13, cleaved caspase‑3 and p21 in IL‑1β‑treated CHON‑001 cells. In addition, IL‑1β induced CHON‑001 cell apoptosis, while SNHG16 knockdown decreased IL‑1β‑induced apoptosis. Furthermore, the luciferase activity assay suggested that SNHG16 negatively regulated miR‑373‑3p in OA. Finally, the results suggested that the proinflammatory effect of IL‑1β on CHON‑001 cells was significantly reduced by SNHG16 knockdown. In conclusion, lncRNA SNHG16 knockdown significantly limited the progression of OA by sponging miR‑373‑3p in vitro, which suggested that SNHG16 may serve as a potential therapeutic target for OA.