Objective: To investigate the effect of a folic acid intervention on the outcome of intrauterine growth restriction (IUGR) filial rats and changes in DNA methyltransferase 1 (DNMT1), growth-associated protein 43 (GAP43), and vascular endothelial growth factor receptor 1 (VEGFR1). Methods: The IUGR animal model was established using a starvation method in pregnant rats. The animals were randomly divided into 4 groups: normal controls, IUGR rats, IUGR rats given folic acid, and IUGR rats given normal saline. After the rats were weighed, the brain tissue was removed and the messenger RNA and protein levels of DNMT1, GAP43, and VEGFR1 were validated by reverse transcription-polymerase chain reaction and western blot. Results: Birth weight was significantly increased after intervention with folic acid compared with the IUGR group, although it remained about 16% lower compared with the normal controls. The expressions of DNMT1 and GAP43, which were significantly upregulated in the IUGR group compared with the normal controls, were decreased with the folic acid intervention. However, there were no significant differences in VEGFR1 expression across groups. Conclusion: Brain damage in IUGR rats mainly manifests as delayed myelination or synaptic maturation and rarely as pathological proliferation of blood vessels. Our results strongly support the idea that the application of folic acid during pregnancy might represent a new epigenetic therapy for IUGR.