Objective: To explore the effects of long intergenic non-coding RNA00707(LINC00707) on interleukin-1β(IL-1β)-induced chondrocyte damage and its molecular mechanism. Methods: Human chondrocytes were treated with 10 ng·ml-1 IL-1β and recorded as IL-1β group; normally cultured cells were used as the control group; the LINC00707 suppression expression vector plasmid(si-LINC00707) and microRNA-224-3p overexpression vector(miR-224-3p) were transfected into chondrocytes and treated with 10 ng·ml-1 IL-1β; the LINC00707 suppression expression vector plasmid and miR-224-3p suppression expression vector plasmid were co-transfected into chondrocytes and treated with 10 ng·ml-1 IL-1β. Real-time fluorescent quantitative PCR(RT-qPCR) was used to measure expression levels of LINC00707 and miR-224-3p, enzyme-linked immunosorbent assay(ELISA) was used to measure interleukin 6(IL-6) and interferon gamma(IFN-gamma) levels, flow cytometry was used to detect cell apoptosis, Western blot was used to characterize protein expression, and the dual luciferase report experiment was used to verify the targeting relationship between LINC00707 and miR-224-3p. Results: Compared with the control group, the LINC00707 expression level was higher in the IL-1β group, the miR-224-3p expression level was lower, IL-6 and IFN-γ levels were lower, the cell apoptosis rate was higher, the expression level of B-cell lymphoma/leukemia-2(Bcl-2) was lower, and the expression level of Bcl-2 related X(Bax) was higher(P<0.05). After inhibiting the expression of LINC00707 or overexpressing miR-224-3p, the levels of L-6 and IFN-γ in chondrocytes induced by IL-1β decreased, the apoptosis rate decreased, the expression of Bcl-2 increased, and the expression of Bax decreased(P<0.05). Down-regulating the expression of miR-224-3p reverses the protective effect of inhibiting the expression of LINC00707 on IL-1β-induced chondrocyte damage. LINC00707 targets and regulates the expression of miR-224-3p. Conclusion: Inhibiting the expression of LINC00707 may inhibit IL-1β-induced chondrocyte damage by targeting the up-regulation of miR-224-3p.
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