Ferulic acid exerts Nrf2-dependent protection against prenatal lead exposure-induced cognitive impairment in offspring mice.

Abstract Prenatal and/or early postnatal exposure to lead (Pb) may be associated with deficits in cognitive function in the toddler offspring, and oxidative stress likely play a central role in mediating these adverse effects. Here, we tested the hypothesis that ameliorative effect of ferulic acid (FA) on lead-induced cognitive deficits attributed to its antioxidant properties in a nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-dependent manner in the context of prenatal Pb exposure. To test this hypothesis, Nrf2 knockout and C57BL/6 wild type mouse dams were exposed/unexposed to PbAc (250 ppm) during gestation day 5 to postnatal day 14 via drinking water, and FA (50 mg/kg)/vehicle was administered orally to dams for 31 d. Spatial learning and memory in pups was assessed by Morris water maze. Biochemical assays, real-time PCR, western blot techniques were employed to evaluate oxidative stress and signaling pathways in the brain of pups. We report that lead acetate (PbAc) leads to deficits in cognitive functions in offspring, which were partially attenuated by FA (P