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缺铁状态下心脏中Nrf2/Keap1信号通路的激活及自噬诱导对氧化应激的抵抗作用

Activation of Nrf2/Keap1 signaling and autophagy induction against oxidative stress in heart in iron deficiency.

作者信息

Inoue Hirofumi, Kobayashi Ken-Ichi, Ndong Moussa, Yamamoto Yuji, Katsumata Shin-Ichi, Suzuki Kazuharu, Uehara Mariko

机构信息

a Faculty of Applied Bioscience, Department of Nutritional Science and Food Safety , Tokyo University of Agriculture , Tokyo , Japan.

出版信息

Biosci Biotechnol Biochem. 2015;79(8):1366-8. doi: 10.1080/09168451.2015.1018125. Epub 2015 Mar 10.

DOI:10.1080/09168451.2015.1018125
PMID:25754743
Abstract

We investigated the effects of dietary iron deficiency on the redox system in the heart. Dietary iron deficiency increased heart weight and accumulation of carbonylated proteins. However, expression levels of heme oxygenase-1 and LC3-II, an antioxidant enzyme and an autophagic marker, respectively, in iron-deficient mice were upregulated compared to the control group, resulting in a surrogate phenomenon against oxidative stress.

摘要

我们研究了饮食缺铁对心脏氧化还原系统的影响。饮食缺铁会增加心脏重量和羰基化蛋白质的积累。然而,与对照组相比,缺铁小鼠体内的血红素加氧酶-1(一种抗氧化酶)和LC3-II(一种自噬标志物)的表达水平上调,从而产生了对抗氧化应激的替代现象。

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