Abstract: Objective To investigate the effect of microRNA(miR)?9a?5p on H2O2?induced neuronal injury and its potential mechanism. Methods PC12 cells were included as the subjects in the study. CCK?8 method and flow cytometry were used to determine the effect of H2O2 treatment on cell proliferation and apoptosis. At the same time,the effect of H2O2 treatment on the release of cellular lactate dehydrogenase(LDH)was examined. The effect of miR?9a?5p overexpression and inhibition of forkhead box protein O1(FOXO1)expression on H2O2?induced PC12 cell injury was determined. The dual luciferase reporter assay identified whether miR?9a?5p targeted FOXO1. The effect of co?expression of miR?9a?5p and FOXO1 on H2O2?induced PC12 cell injury was determined. Results H2O2 treatment of PC12 cells significantly reduced cell viability and the expression level of miR?9a?5p,induced the increase of cell apoptosis and LDH release amount,and promoted mRNA and protein expression levels of FOXO1. Overexpression of miR?9a?5p and inhibition of FOXO1 all reversed the damage of H2O2 to PC12 cells. Overexpression of miR?9a?5p inhibited the expression of FOXO1 in PC12 cells,while the inhibition of miR?9a?5p promoted the expression of FOXO1. Dual luciferase reporter gene assay confirmed that FOXO1 was a negative regulatory target gene of miR?9a?5p. Overexpression of FOXO1 reversed the protective effect of miR?9a?5p overexpression on H2O2?induced PC12 cell injury. Conclusion miR?9a?5p may protect against H2O2?induced neuronal injury by targeted inhibition of FOXO1 expression.