The influence of Hesperidin on memory, learning and oxidative stress parameters in rat model of utreoplacental insufficiency

Abstract

Background: Utreoplacental Insufficiency (UPI) causes impaired fetal brain development and induces oxidative stress, which ultimately leads to intrauterine growth restriction. Due to the antioxidant properties of Hesperidin (HES), the study aimed to outcome this compound on cognitive impairment and serum level of catalase, antioxidant capacity of total and malondialdehyde following uterine-placental insufficiency in rats. Materials and Methods: Thirty pregnant Wistar rats were randomly divided into 5 groups: control group, UPI+NS (Utreoplacental insufficiency+normal saline), UPI+HES25 (Utreoplacental insufficiency+Hesperidin 25 mg/kg), and UPI+HES50 (Utreoplacental insufficiency+Hesperidin 50mg/kg), UPI+HES100 (Utreoplacental insufficiency+ Hesperidin 100mg/kg). UPI was induced by obstruction of the anterior uterine arteries on day 18 of gestation. Hesperidin or normal saline gavage was performed from day 12 to 18 of gestation. Evaluation of working memory, avoidant learning and anxiety-like behaviors and then evaluation of serum levels of catalase, total antioxidant capacity and malondialdehyde content were performed in one-month-old pups. Results: There was a significant decrease in working and avoidance memory, catalase levels, total antioxidants capacity with increased levels of anxiety and malondialdehyde in the UPI+ NS group compared to the control group (P<0.05). While in the HES-treated groups, there was a significant increase in working and avoidance memory, catalase level and total antioxidant capacity with a decrease in anxiety and malondialdehyde levels compared to the UPI+NS group (P<0.05(. Conclusion: Hesperidin can improve memory and cognitive impairments in the model of uterine-placental insufficiency of rats by reducing oxidative stress damage.

Keywords

• intrauterine growth retardation
• hesperidin
• oxidative stress
• anxiety
• memory-short term
• rat