乙醇暴露在产前和产后早期诱导的大鼠心脏损伤中:在为期 3 个月的随访研究中,氧化应激、Hsp70、ERK 1/2、JNK 和细胞凋亡的参与。

Cell Stress and Chaperones Pub Date : 2019-09-01 Epub Date: 2019-08-13 DOI:10.1007/s12192-019-01015-w
Alireza Shirpoor, Reza Gaderi, Roya Naderi
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引用次数: 0

摘要

妊娠期间接触酒精会诱发胎儿心脏出现各种结构和功能异常。然而,这一现象的内在机制尚不清楚。本研究旨在阐明产前和产后早期乙醇治疗诱发心肌损伤的可能机制。妊娠 Wistar 大鼠从妊娠第七天(GD7)开始,每天接受一次每公斤体重 4.5 克的乙醇,直至整个哺乳期。通过测量氧化应激生物标志物的水平来评估幼鼠心肌的氧化应激损伤。对出生后第 21 天(PN-21)和出生后第 90 天(PN-90)雄性幼崽心肌组织的组织病理学特征、细胞凋亡和分子改变进行了组织病理学检查和 Western 印迹检测。结果表明,母体摄入乙醇会导致出生后第 21 天和出生后第 90 天幼鼠心肌组织的氧化应激(总抗氧化能力和丙二醛受损)、组织学变化和凋亡。在分子水平上,Western 印迹分析显示,与对照组相比,乙醇调节了出生 21 天和 90 天后幼鼠心肌组织中 p-ERK1/2、p-JNK 和 Hsp70 的蛋白表达。这些研究结果表明,母体摄入乙醇会诱发幼鼠心脏毒性,部分是由氧化应激和细胞凋亡介导的。进一步的机理研究显示,乙醇增强了ERK1/2和JNK磷酸化以及Hsp70蛋白的表达。
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Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study.

Alcohol exposure during pregnancy induces a wide range of structural and functional abnormalities in the fetal heart. However, the underlying mechanism of this phenomenon is not well known. This study was undertaken to elucidate probable mechanisms of myocardial damage induced by prenatal and early postnatal ethanol treatment. Pregnant Wistar rats received ethanol 4.5 g/kg BW once per day from the seventh day of gestation (GD7) throughout lactation. The oxidative stress injury of the myocardium in pups was evaluated by measuring levels of oxidative stress biomarkers. Histopathological examinations and Western blot were performed to evaluate histological features, apoptosis, and molecular alterations in the myocardial tissue of male pups on the postnatal day 21 (PN-21) and postnatal day 90 (PN-90). The results showed that maternal ethanol consumption caused oxidative stress (impaired total antioxidant capacity and malondialdehyde), histological changes, and apoptosis of the myocardium in the pups on PN-21 and PN-90. At the molecular levels, Western blot analysis revealed that ethanol modulated the protein expression of p-ERK1/2, p-JNK, and Hsp70 in the myocardial tissue of the pups after 21 and 90 days of birth compared with the controls. These findings revealed that maternal ethanol intake induced cardiac toxicity in part, mediated by oxidative stress and apoptosis in the pups. A further mechanism study revealed that ethanol enhanced ERK1/2 and JNK phosphorylation and Hsp70 protein expression.

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