4.7 Article

Effect of Postnatal Epigallocatechin-Gallate Treatment on Cardiac Function in Mice Prenatally Exposed to Alcohol

Journal

ANTIOXIDANTS
Volume 12, Issue 5, Pages -

Publisher

MDPI
DOI: 10.3390/antiox12051067

Keywords

FASD-like mouse model; prenatal alcohol exposure (PAE); binge alcohol drinking pattern; moderate alcohol drinking pattern; heart; echocardiography; oxidative stress; apoptosis; natural; antioxidants; epigallocatechin-3-gallate (EGCG)

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Prenatal alcohol exposure can cause cardiovascular health issues in offspring. This study investigated the effects of the compound EGCG on cardiac dysfunction in mice prenatally exposed to alcohol. The results showed that prenatal alcohol exposure led to cardiac alterations and dysfunction, but postnatal treatment with EGCG restored physiological levels of heart biomarkers and improved cardiac function. These findings suggest that postnatal EGCG treatment can attenuate the damage caused by prenatal alcohol exposure.
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 Hif1 alpha 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.

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