| objective:To explore the regulatory effect and mechanism of long-chain non-coding RNA SNHG1 on interleukin 1β(IL-1β)-induced chondrocyte inflammation injury.Methods:IL-1β was used to induce primary cultured mouse chondrocytes to establish an inflammatory injury model.Chondrocytes were treated with different concentrations of IL-1β(0,1,5,10 ng / ml),MTT assay was used to determine cell viability,and qRT-PCR was used to determine the relative expression levels of inflammatory factors and SNHG1.The biological function of SNHG1 overexpression or inhibition in IL-1β injured chondrocytes was also evaluated.Then,the possible SNHG1 target was screened through an online database(Starbase),and the relationship between SNHG1,miRNA-143-3p and Krüppel-like factor 2(KLF2)was verified by qRT-PCR and luciferase reporter gene experiments.At the same time,the influence of abnormal expression of downstream target genes on the regulation of SNHG1 in inflammatory injury induced by IL-1β was also detected by qRT-PCR,Western blot and flow cytometry.Results:SNHG1 was reduced in mouse chondrocytes induced by IL-1β.Moreover,overexpression of SNHG1 reduced apoptosis,inhibited the inflammatory response and the degradation of extracellular matrix(ECM).Knocking down SNHG1 obtained the opposite results.Mechanistically,SNHG1,which functions as a sponger,directly bound to miRNA-143-3p,and miRNA-143-3p suppressed SNHG1 expression.Additionally,transfection of miRNA-143-3p mimics reversed the inhibition of apoptosis and ECM degradation exerted by SNHG1 overexpression.Furthermore,KLF2 was a target gene of miRNA-143-3p,the expression of KLF2 induced by SNHG1 was markedly reversed by the introduction of miRNA-143-3p.Finally,the data of recovery experiments indicated that SNHG1 exerts its function by indirectly regulating the downstream target KLF2 of miRNA-143-3p.Conclusion:Our study demonstrated that lncRNA SNHG1 alleviated the IL-1β-induced chondrocytes inflammatory injury by targeting miRNA-143-3p / KLF2 axis.It is suggested that SNHG1 might be a potential therapeutic target in OA. |