Andreu-Fernández Vicente, Serra-Delgado Mariona, Almeida-Toledano Laura, García-Meseguer Àgueda, Vieiros Melina, Ramos-Triguero Anna, Muñoz-Lozano Concha, Navarro-Tapia Elisabet, Martínez Leopoldo, García-Algar Óscar, Gómez-Roig María D
Grup de Recerca Infancia i Entorn (GRIE), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain.
Biosanitary Research Institute, Valencian International University (VIU), 46002 Valencia, Spain.
Antioxidants (Basel). 2023 May 9;12(5):1067. doi: 10.3390/antiox12051067.
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.
孕期酒精暴露会影响子代的心血管健康。表没食子儿茶素-3-没食子酸酯（EGCG）可能是一种针对此情况的保护剂，但尚无关于其对心脏功能障碍影响的数据。我们研究了孕期暴露于酒精的小鼠心脏改变的存在情况，以及产后EGCG治疗对心脏功能和相关生化途径的影响。C57BL/6J怀孕小鼠在怀孕第19天前接受1.5 g/kg/天（地中海模式）、4.5 g/kg/天（暴饮模式）的乙醇或麦芽糊精。分娩后，治疗组饮用补充了EGCG的水。在出生后第60天，进行功能性超声心动图检查。通过蛋白质印迹法分析凋亡、氧化应激和心脏损伤的心脏生物标志物。产前暴露于地中海酒精模式的小鼠中，脑钠肽（BNP）和低氧诱导因子1α（Hif1α）增加，核因子E2相关因子2（Nrf2）减少。在暴饮式孕期酒精暴露模式中，B细胞淋巴瘤-2（Bcl-2）下调。在两种乙醇暴露模式下，肌钙蛋白I、谷胱甘肽过氧化物酶和 Bax均增加。产前酒精暴露导致暴露小鼠出现心脏功能障碍，表现为射血分数降低、舒张期左心室后壁厚度和Tei指数降低。产后EGCG治疗恢复了这些生物标志物的生理水平并改善了心脏功能障碍。这些发现表明，产后EGCG治疗可减轻子代中产前酒精暴露所致的心脏损伤。
