Abstract
Changes in glucose metabolism of diabetic mothers affect immunological components, proinflammatory factors, and placental hypervascularization that can induce cell death. The hormone melatonin has been identified as a potential modulating agent. The aim of this study was to analyze the oxidative process and the apoptosis in maternal blood and placental cells modulated by melatonin from diabetic mothers. The groups were 40 pregnant women divided into non-diabetic (ND) and type 2 diabetes mellitus (T2DM) groups. Blood and placental cells were obtained by density gradient and maintained in culture treated or not with melatonin (100 ng/mL) for 24 h (37°C, 5% CO2). Oxidative stress was evaluated by superoxide release and CuZn superoxide dismutase (SOD). Apoptosis was assessed by flow cytometry. Maternal hyperglycemia increased superoxide release and apoptosis in MN cells from maternal blood and reduced SOD level and SOD/O2- ratio. Melatonin reduced oxidative stress and apoptosis rates in MN cells in the blood of diabetic mothers. There was a reduction in SOD and SOD/O2- ratio in the placental extravillous layer, and melatonin restored the concentrations of this enzyme. There was greater superoxide release, reduced SOD/O2- ratio, and apoptosis in MN cells placental villous layer. Melatonin increased apoptosis rates in the placental villous layer from hyperglycemic mothers. These data suggest that hyperglycemia altered the processes oxidative in blood and placenta from hyperglycemic mothers. These changes reflected in the mechanisms of induction of apoptosis, especially in the vascularized layers of the placenta, and were modulated by melatonin.
Highlights
The placenta is a highly vascularized transitory organ from fetal–maternal tissues that play important functions in maintaining pregnancy and promoting fetal development (Moore and Persaud, 2008)
Hyperglycemia maternal promotes the production of reactive oxygen species (ROS), resulting in oxidative stress, which can contribute to the proinflammatory environment typical of diabetes (Cvitic et al, 2014) and placental hypervascularization, with alterations in vasculogenesis and VEGF-R1 and R2 receptors
P < 0.05 statistical difference (ANOVA test) ∗ comparing the groups considering the same treatment and type of sample; # comparing untreated cells with cells treated with melatonin, considering the same group and sample; †comparing between villous and extravillous placental layers considering the same treatment and group
Summary
The placenta is a highly vascularized transitory organ from fetal–maternal tissues that play important functions in maintaining pregnancy and promoting fetal development (Moore and Persaud, 2008). This organ plays a critical role in immunoregulation (Hara et al, 2016) and sources cells from maternal and fetal origin. These cells present molecules that have an essential role in maternal–fetal tolerance (Guleria and Sayegh, 2007). Maternal hyperglycemia may trigger structural and physiological responses to assure maternal–fetal exchanges and fetal oxygen delivery and alter cellular oxidative metabolism at the maternal–fetal interface (Gauster et al, 2011) with an imbalance between the generation of reactive oxygen species (ROS) and antioxidant defense
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