Abstract:Objective To investigate the effect of miR-449a on the apoptosis of osteoarthritis (OA) chondrocytes and its mechanism.Methods Human normal chondrocytes and OA chondrocytes were isolated and cultured in vitro. The expression of miR-449a was detected by realtime fluorescence quantitative PCR. The OA chondrocytes cultured in vitro were divided into miR449a mimics group (transfected with miR-449a mimics), miRNC group (transfected with miR-449a mimics negative control), miR-449a inhibitor group (transfected with miR-449a inhibitor) and inhibitor NC group (transfected with miR-449a inhibitor negative control). The expression of miR-449a in each group was detected by realtime fluorescent quantitative PCR, and the apoptosis rate of each group was detected by flow cytometry. The target relationship between miR-449a and DeltaLike1 (DLL1) was detected by double luciferase reporter gene assay, and the effect of miR-449a on DLL1 protein expression was detected by Western blotting.DLL1 interference sequence siRNADLL1 and DLL1 overexpression plasmid GFPDLL1 were transfected to construct OA soft bone cells with low and over expression of DLL1. The effect of DLL1 on apoptosis of OA chondrocytes was observed.Results Compared with human normal chondrocytes, the expression level of miR449a in OA chondrocytes increased significantly (P<0.05). Compared with mimic-NC group, miR449a expression level and apoptosis rate in miR-449a mimic group were significantly higher, while miR449a expression level and apoptosis rate in miR-449a inhibitor group were significantly lower than those in inhibitor- NC group (P<0.05). DLL1 was a potential target gene of miR449a, and miR449a could negatively regulate DLL1 protein expression. DLL1 was a low expression OA chondrocyte apoptosis rate The apoptosis rate of OA chondrocytes in siRNANC group was significantly higher than that in GFP group (P<0.05).Conclusion miR-449a can promote apoptosis of OA chondrocytes by targeting DLL1 expression