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The effect of Gallic acid on fetus viability and hippocampal cell damages in rat model of utreo-placental insufficiency
Mohammad Yousefi-Ghalati Mr. , Mohammad Amin Edalatmanesh Dr. * 1
1- , amin.edalatmanesh@gmail.com
Abstract:   (63 Views)
Introduction
Uteroplacental insufficiency (UPI) causes brain damage and neurodevelopmental deficits in intrauterine growth-restricted fetus. This study examined the effect of Gallic acid (GA) on fetus viability and weight of fetus, uterus, and placenta and hippocampal piramidal cell densityof fetus in UPI model.
Materials and Methods
25 pregnant Wistar rats were randomly divided into 5 groups: control, UPI+NS (Uteroplacental insufficiency + Normal saline), UPI+GA100 (Uteroplacental insufficiency + Gallic acid 100), UPI+GA200 (Uteroplacental insufficiency + Gallic acid 200) and UPI+GA400 (Uteroplacental insufficiency + Gallic acid 400). UPI induction is carried out by anterior uterine artery occlusion on gestation day (GD) 18. GA or normal saline was administrated by gavage method from GD15 to GD21. Then, on GD21 the fetus were cesarean section and after weighing, anesthetized by hypothermia, their heads were cut and the brains evaluated for histopathological studies.
Results
A significant increase in uterine weight and a significant decrease in fetal viability and cell density were observed in the hippocampal CA1, CA2 and CA3 subdivision in UPI+NS group compared to the control group (p˂0.05). On the other hand, viability rate, fetus weight and cell density in CA1 and CA3 subdivisions were significantly higher in the GA-treated groups than the UPI+NS group (p˂0.05).
  Conclusion
GA reduced fetal mortality and fetal hippocampal cell damage in UPI model. Therefore, it usable to avoid the neurodevelopmental complications due to intrauterine growth restriction.
Keywords: Gallic acid, Fetal Growth Retardation, Brain injuries, Hippocampus, Fetal viability
     
Type of Study: Orginal Article | Subject: Physiology
Received: 2019/07/24 | Revised: 2019/09/22 | Accepted: 2019/09/24 | ePublished ahead of print: 2019/11/1
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