The effect of cinnamic acid on fetal hippocampus in pregnant rats

Abstract

Uteroplacental insufficiency (UPI) causes neurodevelopmental deficits in the brain of intrauterine growth-restricted offspring, even though the mechanisms are equivocal. The most important factor in these deficits is oxidative stress. Cinnamic acid (CA) and derivatives have been described to exhibit antioxidant activity. In this study, the researchers examined the neuroprotective effect of CA on the parameters of oxidative stress and hippocampal cell density in the UPI rat model. In this experiment, the Wistar rats were mated, and UPI was induced at gestation day (GD) 18. For UPI induction, anterior uterine artery occlusion surgery is conducted in deep anesthesia. From GD15, CA was administrated orally in 25, 50, and 100 mg/kg BW doses until GD21. GD21 evaluated the weight of the uterine, placenta, and embryo. Also, the oxidative stress parameters in the hippocampus, e.g., catalase activity (CAT), total antioxidant activity (TAC), and malondialdehyde (MDA), were measured using the ELISA technique in the fetus. Finally, the cell density of the fetal hippocampus was estimated using the histopathological method. CA reduces the MDA at various concentrations and increases CAT and TAC in comparison with the untreated group (p ˂ 0.001). Besides, the cell density of CA3 and CA4 as hippocampus subareas are significantly increased than the untreated group, especially in the UPI + CA100 group (p = 0.002 and p = 0.001, respectively). Our data revealed that CA ameliorated the oxidative stress parameters and hippocampal cell damages in the UPI rats. Therefore, the CA can have neuroprotective effects in UPI model.