Abstract
The study evaluated the effect of the supernatant of placental explants from preeclamptic (PE) and normotensive (NT) pregnant women after tissue treatment with or without vitamin D (VD) on oxidative stress and nitric oxide (NO) bioavailability in human umbilical vein endothelial cells (HUVEC). Placental explants were prepared from eight NT and eight PE women, and supernatants were obtained after incubation with or without hydrogen peroxide (H2O2) and/or VD. HUVEC were cultured for 24 h with supernatants, and the following parameters were analyzed in HUVEC cultures: NO, nitrate (NO3 -), and nitrite (NO2 -) levels, lipid peroxidation, and intracellular reactive oxygen species (ROS). Results showed that the production of NO3 -, NO2 -, malondialdehyde (MDA), and ROS were significantly higher in HUVEC treated with explant supernatant from PE compared to NT pregnant women, while the supernatant of PE explants treated with VD led to a decrease in these parameters. A significantly high production of NO was detected in HUVEC cultured with control supernatant of NT group, and in cultures treated with supernatant of PE explants treated with VD. Taken together, these results demonstrated that cultures of placental explants from PE women with VD treatment generated a supernatant that decreased oxidative stress and increased the bioavailability of NO in endothelial cells.
Highlights
Preeclampsia (PE) is a specific human syndrome of pregnancy characterized as the main cause of morbidity, mortality, and preterm birth, affecting as many as 10% of all pregnancies
Considering that the placenta of women with PE shows oxidative stress, exacerbated inflammation, and Nitric oxide (NO) system imbalance, this study aimed to evaluate the effect of the supernatant of placental explants from PE and NT pregnant women treated with or without vitamin D (VD) on oxidative stress and NO bioavailability in human umbilical vein endothelial cells (HUVEC)
We demonstrated that placental explants from PE women cultured without stimulus produced endogenous levels of the proinflammatory cytokines IL-1b, tumor necrosis factor (TNF)-a, and IL-18
Summary
Preeclampsia (PE) is a specific human syndrome of pregnancy characterized as the main cause of morbidity, mortality, and preterm birth, affecting as many as 10% of all pregnancies. Nitric oxide (NO) is a key signaling molecule in the cardiovascular system, controlling vascular tone, neurotransmission, redox signaling, cellular respiration, and host defense [3]. This molecule participates actively in the pregnancy processes such as trophoblast invasion and placental development, representing the main vasodilator in the placenta [4]. Oxidative stress, characterized by excessive formation of reactive oxygen species (ROS), can impair endothelial nitric oxide synthase (eNOS) function [6] and decrease bioavailability of NO. Together with the excessive production of ROS, the placenta from preeclamptic women shows an intense inflammatory process. ROS are involved in the injuries signaling to the immune system [7] and can orchestrate the inflammatory response by the release of hydrogen peroxide (H2O2)
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