Preeclampsia (PE) is a leading cause of stroke and cognitive impairment in the offspring. Melatonin is involved in the outcome of normal pregnancy. Its receptors are widespread in the embryo. This study aimed to investigate the fetal neuroprotective effect of melatonin in experimentally induced PE. After induction of pregnancy in 18 female rats, they were divided into three equal groups. PE was induced in groups II and III by injection of deoxycorticosterone acetate and drinking isotonic saline. Melatonin was supplied to group III orally (10 mg/kg body weight) throughout pregnancy. Pregnancy was terminated on day 20, and macroanatomical investigation of three fetuses from each pregnant rat and their placentae was performed. Placental and brain homogenates were analyzed for malondialdehyde (MDA), placental growth factor (PLGF), tumor necrosis factor-α (TNF-α), and brain transforming growth factor-β (TGF-β). Histopathological analysis of fetal brain sections was performed. Melatonin improved placental, fetal, and brain weight; significantly reduced fetal death rate; significantly increased PLGF, placental and brain superoxide dismutase, and brain TGF-β; and significantly decreased placental TNF-α and brain MDA. Brain micromorphological study found normal glial cells and neuropil in the melatonin-treated group and a loss of neuronal cell outlines with an accumulation of cellular debris in the untreated group. In conclusion, melatonin approximately showed a neuroprotective activity by managing PE-induced oxidative stress in the placenta and fetal cerebral cortex of rats.