Objective To investigate the mechanism of vitexin in reversing isoflurane-induced nerve damage. Methods The isoflurane-induced nerve injury SD rats were constructed and divided into five groups: the model group, the vitexin low, medium, and high dose groups and the control group. Morris water maze experiment were used to evaluate the memory ability of model rats, the expression of miR-409 in hippocampus were detected by qPT-PCR, the cell apoptosis of hippocampus cells were detected by TUNEL methods. Results Vitexin could shorten the escape latency (ELP) of rats in the model group and significantly increase the expression of miR-409, inhibit apoptosis(P<0.05,P<0.01）. Conclusion Vitexin reverses the neurotoxicity induced by isoflurane by targeting miR-409 pathways.