Objective To observe the effects of Xingnaozaizao capsule on formaldehyde-induced impairment of memory and preliminarily explore the mechanisms in mice. Methods Specific pathogen-free healthy KM mice were randomly divided into blank control, solvent control, and low-, medium- and high-dose groups with 14 mice in each group. The groups of mice, except the blank control group, were placed in a formaldehyde poisoning device for 14 days. The latency and number of errors in a step-through test were observed. The activities of nitric oxide synthase (NOS) and superoxide dismutase (SOD), and the content of malonaldehyde (MDA) in brain tissue were measured biochemically. The number and morphology of pyramidal neurons in the mouse hippocampal CA1 area were observed after HE staining. Results Compared with the blank control group, the latency was shortened ( P <0. 01), the number of errors was increased ( P <0. 01), NOS and SOD activities in brain tissue were decreased ( P <0. 05), and the content of MDA was increased ( P <0. 01) in the solvent control group. The numbers of piramidal cells were reduced, cell arrangement was sparse and disordered, and the cell shape was irregular in the CA1 area of the hippocampus in the solvent control group. Compared with the solvent control group, the latencies of medium- and high-dose groups were lengthened ( P < 0. 05) and the numbers of errors in low-, medium- and high-dose groups were decreased ( P <0. 05). The activities of NOS and SOD were increased in brain tissues of medium- and high-dose groups ( P < 0. 01). The contents of MDA were decreased in brain tissues of low-, medium- and high-dose groups ( P < 0. 01). The layers of pyramidal neurons in the mouse hippocampalCA1 area were increased slightly in the low- and medium-dose groups. The layers of pyramidal neurons were clear, cell arrangement was compact, and the numbers of cells were increased in the CA1 area of the hippocampus in the high-dose group. Conclusions Xingnaozaizao capsule improves formaldehyde-induced impairment of memory in mice. Its mechanisms may be associated with the effects of antioxidant injury and an increased number of pyramidal neurons in the CA1 area of the hippocampus.