Evaluation of the effect of exogenous melatonin on the placenta and inflammatory cytokines in rats submitted to chronic alcohol consumption.

Abstract

Global alcohol consumption by pregnant women is approximately 9.8%. This consumption can hinder the interaction of the placenta with the fetus and increase levels of oxidative stress by altering and deregulating the expression of cytokines, leading to complications such as slow intrauterine development, such as low birth weight, premature babies and even stillbirths. It is known that melatonin is a natural antioxidant that acts mainly on the liver and also on various organs such as the ovary, placenta and the fetus itself. Melatonin can freely cross the placenta and exert effects on the mother and fetus. The present work aimed to analyze the effects of exogenous administration of melatonin during pregnancy on the placenta of rats subjected to chronic alcohol consumption. 30 albino rats were used, divided into 3 groups: Control - 10 pregnant rats that will not receive alcohol; Alcohol - 10 pregnant rats subjected to chronic alcohol consumption; Alcohol + Melatonin - 10 pregnant rats subjected to alcohol consumption associated with melatonin. Alcohol was administered at a dose of 3g/kg by gavage, while melatonin was administered at night at a dose of 0.8mg/kg intraperitoneally. The placentas were weighed and analyzed histopathologically, morphometrically and immunohistochemically. The results showed a significant reduction in placental weight in the alcohol group, disorganization in the labyrinthine zone and reduction of maternal and fetal vessels in the alcohol group. There was strong staining for TNF α and VEGF factors in the alcohol group. And as for PCNA, the control group and the alcohol + melatonin group showed the highest percentages of positive cells. And in relation to apoptosis, there was strong staining in the junctional zone of the placentas of females in the alcohol group. Therefore, it is concluded that melatonin has the potential to protect against the oxidative damage of ethanol in placental cells and can also regulate the generation of inflammatory cytokines.