RESUMEN
Prenatal alcohol exposure affects the cardiovascular health of the offspring. Epigallocatechin-3-gallate (EGCG) may be a protective agent against it, but no data are available regarding its impact on cardiac dysfunction. We investigated the presence of cardiac alterations in mice prenatally exposed to alcohol and the effect of postnatal EGCG treatment on cardiac function and related biochemical pathways. C57BL/6J pregnant mice received 1.5 g/kg/day (Mediterranean pattern), 4.5 g/kg/day (binge pattern) of ethanol, or maltodextrin until Day 19 of pregnancy. Post-delivery, treatment groups received EGCG-supplemented water. At post-natal Day 60, functional echocardiographies were performed. Heart biomarkers of apoptosis, oxidative stress, and cardiac damage were analyzed by Western blot. BNP and Hif1α increased and Nrf2 decreased in mice prenatally exposed to the Mediterranean alcohol pattern. Bcl-2 was downregulated in the binge PAE drinking pattern. Troponin I, glutathione peroxidase, and Bax increased in both ethanol exposure patterns. Prenatal alcohol exposure led to cardiac dysfunction in exposed mice, evidenced by a reduced ejection fraction, left ventricle posterior wall thickness at diastole, and Tei index. EGCG postnatal therapy restored the physiological levels of these biomarkers and improved cardiac dysfunction. These findings suggest that postnatal EGCG treatment attenuates the cardiac damage caused by prenatal alcohol exposure in the offspring.
RESUMEN
BACKGROUND: Maternal exposure to air pollution has been associated with poor obstetric outcomes. However, the available evidence on the impact of maternal exposure to air pollution on placental function is still scarce and is based on estimated ambient levels of air pollutants. OBJECTIVE: To evaluate the association between short-term maternal exposure to NO2 based on the objective personal measure of NO2 exposure and Doppler markers of placental function. METHODS: This study was based on a prospective cohort of 101 pregnant women, recruited at Hospital Sant Joan de Déu, Barcelona (Spain), between January 2017 and April 2018. NO2 diffusion tubes were worn by pregnant women to measure personal exposure to NO2 between weeks 28 and 32 of their pregnancy. Placental function was evaluated at the 32nd week of gestation by Doppler evaluation of mean uterine arteries pulsatility index (PI), umbilical artery PI, middle cerebral artery PI, cerebroplacental ratio (CPR) and ductus venosus PI. Linear regression models were applied to estimate the association of personal NO2 exposure and Doppler markers of placental function (one at a time), controlled for relevant covariates. RESULTS: Higher personal exposure to NO2 was significantly associated with lower mean uterine artery PI. Each one-interquartile range (IQR) increase in the exposure to NO 2 was associated with -0.07 (95% confidence intervals (CIs): -0.12, -0.02) decrease in uterine arteries PI. We also observed some suggestions for an inverse association between this exposure and CPR. A one-IQR increase in NO2 was associated with -0.18 (95% CIs: -0.37, 0.01) decrease in CPR. The findings for the rest of Doppler markers were not conclusive. CONCLUSIONS: Maternal exposure to NO2 could interfere with Doppler markers of placental function, potentially indicating a certain degree of cerebral vasodilatation with a decrease of mean uterine arteries PI.
