| Objective To explore the effect and mechanism of hsa_circ_0005105 on the proliferation, apoptosis and secretion of inflammatory factors of arthritis chondrocytes. Methods Real-time fluorescent quantitative PCR (RT-qPCR) was used to detect the expression levels of hsa_circ_0005105 and miR-508-3p in chondrocytes; chondrocytes were divided into NC group, IL-1β group, IL-1β+si-NC group, IL-1β+si-hsa_circ_0005105 group, IL-1β+miR-NC group, IL-1β+miR-508-3p group, IL-1β+si-hsa_circ_0005105+anti-miR-NC group, IL-1β+si-hsa_circ_ 0005105+anti-miR-508-3p group; apoptosis protein expression was detected by Western blotting; apoptosis was detected by flow cytometry; CCK-8 and plate clone formation ability were used to detect cell proliferation ability; enzyme-linked immunosorbent assay to detect levels of TNF-α and IL-6; dual luciferase reporter experiment to detect the targeting relationship between hsa_circ_0005105 and miR-508-3p. Results The expression level of hsa_circ_0005105 in IL-1β-induced chondrocytes was increased, and the expression level of miR-508-3p was decreased (P<0.05). Low expression of hsa_circ_0005105 or overexpression of miR-508-3p could reduce the relative expression levels of Bax, Cleaved-caspase-9 and Cleaved-caspase-3, and the apoptosis rate of chondrocytes induced by IL-1β, and increase the level of Bcl-2 protein, Cell viability, the number of cell clones increased, and the levels of TNF-α and IL-6 decreased (P<0.05). hsa_circ_0005105 targets and regulates miR-508-3p; low expression of miR-508-3p could reverse the effect of low expression of hsa_circ_0005105 on IL-1β-induced chondrocyte damage and inflammatory factor secretion. Conclusions The low expression of hsa_circ_0005105 can inhibit IL-1β-induced chondrocyte apoptosis and secretion of inflammatory factors by targeting up-regulation of miR-508-3p, and promote cell proliferation. |