Objective To investigate the effect of Bone Morphogenetic Protein 7(BMP-7)on glucocorticoid(GC)-induced apoptosis in PC12 cells.Methods PC12 cells were treated with different concentrations of GC to determine the impact of GC on apoptosis.PC 12 cells were then infected with BMP7 overexpression/knockdown lentivirus or control virus.Subsequently,cells were treated with DMSO or GC,and apoptosis levels were assessed using flow cytometry.Real-time quantitative polymerase chain reaction(qRT-PCR)was employed to measure Bax gene expression,and Western blotting was used to evaluate Cleaved-Caspase-3 protein expression.Results There were statistically significant differences in apoptosis rate,Bax gene expression,and Cleaved-Caspase-3 protein expression among cells treated with different concentrations of GC(P<0.05).Compared to 0 μmol/L GC,PC12 cell apoptosis significantly increased at a GC concentration of 10 μmol/L(P<0.05),and at a concentration of 50 μmol/L,Bax gene expression and Cleaved-Caspase-3 protein expression increased(P<0.05).Apoptosis rate,Bax gene expression,and Cleaved-Caspase-3 protein expression differed significantly among the four groups with BMP-7 overexpression or knockdown(P<0.05).Compared to the GC-negative control(GC-NC)group,cells in the GC-overexpressing BMP-7 group showed decreased apoptosis,Bax gene expression,and Cleaved-Caspase-3 protein expression(P<0.05).No significant differences were observed in apoptosis level,Bax gene expression,and Cleaved-Caspase-3 protein expression between the GC-overexpressing BMP-7 group and the DMSO-negative control(DMSO-NC)group(P>0.05).In comparison to the DMSO-NC group,cells in the DMSO-knockdown BMP-7 group exhibited increased apoptosis,Bax gene expression,and Cleaved-Caspase-3 protein expression(P<0.05).The GC-knockdown BMP-7 group showed a significant increase in apoptosis level,Bax gene expression,and Cleaved-Caspase-3 protein expression compared to the GC-NC group(P<0.05).Conclusion High levels of GC induce increased apoptosis in PC12 cells,and BMP-7 can counteract GC-induced apoptosis.