Background: Osteoarthritis (OA) was a chronic degenerative joint disease. The dysregulation of circular RNAs (circRNAs) has been identified in OA progression. However, the function and regulation mechanism of circ_0114876 in OA remains largely unknown. Method: Firstly, we used LPS-treated £28/I2 cells as a cellular model of OA. Quantificational real-time poly- merase chain reaction (qRT-PCR) was used to determine tile expression levels of circ_0114876, miRNA-1227-38 and ADAM10 in OA chondrocytes. Cell Counting Kit-8 (CCKB), 5-ethynyl-20-deoxyuridine (EdU) incorporation assays, flow cytometry, Enzyme-linked immunosorbent assay (ELISA) kit, and western blot were applied to confirm cell proliferation, apoptosis, inflammation, and extracellular matrix. of circ_0114876 in vitro. The interaction between cim_0114876 and its downstream target (miR-1227-3p) and mRNA target ADAM metallopeptidase domain 10 (ADAM10), was evaluated by luciferase assay and RNA immunoprecipitation (RIP) assay Result.· Circ-0114876 and ADAM10 were upregulated and miR-1227-3p was decreased in OA tissues and LPStreated chondrocytes. Low expression of cim_0114876 promoted proliferation and inhibited apoptosis, inflammation, and extracellular matrix of the LPS-treated chondrocytes. Mechanistically, circ_01 14876 functioned in human chondrocytes through targeting miR-1227-3p and ADAM10. Furthermore, miRNA-1227-3p inhibitor reversed the effect of circ_0114876 knockdown on the OA chondrocytes, and ADAM10 overexpression reversed the effect of miR-1227-3p mimic on the OA cliondrocytes. Conclusion: Cim_01 14876 was increased in OA tissues and cells. Circ_01 14876 facilitated the progression in the LPS-induced OA cell model via regulating the miR-1227-3p/ADAM10 axis. This study would provide a potentially effective Lherapeutic strategy for OA progression. [ABSTRACT FROM AUTHOR]