Abstract:Objective To investigate the effects of miR-33b-3p on chondrocyte cell proliferation, apoptosis, and ECM degradation.Methods MiR33b3p mimics and miR-33b-3p inhibitors were transfected into chondrocytes. The proliferationof chondrocytes was detected by the CCK-8 method, and the percentage of chondrocyte apoptosis was measured by flow cytometry,RTPCR and Western blot experiments were performed to detect the expression of CyclinD1, CyclinE1, p21, and apoptosisrelated proteins Bcl-2, caspase 9,and Bax, and ECM degradationrelated proteins TIMPs, MMP-9,and EMMPRIN. Analysis of dual luciferase activity CDKN1A was an experimental target for miR-33b-3p. The constructed overexpressing pcDNA3.1CDKN1A plasmid was transfected into chondrocytes, and the expression levels of CyclinD1, CyclinE1, p21, Bcl-2, caspase-9, Bax and TIMPs, MMP-9 and EMMPRIN in chondrocytes were detected by Western blot experiments.Results Compared with chondrocytes, miR-33b-3p mimic group cells were significantly reduced. The flow cytometry detected a significantly increased number of apoptotic cells in miR-33b-3p mimic group. CyclinD1,CyclinE1 expression decreased. ,p21 expression increased. Bcl-2 expression decreased. Caspase 9 and Bax expression increased. TIMPs expression increased. MMP9 and EMMPRIN expression decreased. miR33b3p targeted CDKN1A3′UTR. After overexpression of pcDNA3.1CDKN1A plasmid, it can promote chondrocyte proliferation, inhibit cell apoptosis, and promote ECM degradation.Conclusion miR-33b-3p can inhibit the proliferation of chondrocytes, promote the apoptosis of chondrocytes, and inhibit the degradation of ECM of chondrocytes by targeting the 3′UTR of CDKN1A gene.