Pre-treatment of rats with ad-hepcidin prevents iron-induced oxidative stress in the brain
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摘要Our recent investigation showed that hepcidin can reduce iron in the brain of iron-overloaded rat by down-regulating iron-transport proteins. It has also been demonstrated that iron is a major generator of reactive oxygen species. We therefore hypothesized that hepcidin could prevent iron accumulation and thus reduce iron-mediated oxidative stress in iron-overloaded rats. To test this hypothesis, we investigated the effects of pre-treatment of rats with recombinant-hepcidin-adenovirus (ad-hepcidin) on the contents of iron, dichlorofluorescein and 8-isoprostane in the brain. Hepcidin expression was detected by real-time PCR and immunofluorescence analysis. Iron contents were measured using Perl's staining as well as graphite furnace atomic absorption spectrophotometry. Dichlorofluorescein and 8-isoprostane were determined using a fluorescence spectrophotometer and an ELISA kit, respectively. We found that hepcidin contents in the cortex, hippocampus, striatum and substantia nigra of rats treated with ad-hepcidin are 3.50, 2.98, 2.93 and 4.07 fold of those of the control rats respectively. Also, we demonstrated that the increased iron as well as dichlorofluorescein and 8-isoprostane levels in all four brain regions, induced by injection of iron dextran, could be effectively prevented by pre-treatment of the rats with ad-hepcidin. We concluded that pre-treatment with ad-hepcidin could increase hepcidin expression and prevent the increase in iron and reduce reactive oxygen species in the brain of iron-overloaded rats. (C) 2015 Elsevier Inc. All rights reserved.
著者Gong J, Du F, Qian ZM, Luo QQ, Sheng Y, Yung WH, Xu YX, Ke Y
期刊名稱Free Radical Biology and Medicine
出版年份2016
月份1
日期1
卷號90
出版社ELSEVIER SCIENCE INC
頁次126 - 132
國際標準期刊號0891-5849
電子國際標準期刊號1873-4596
語言英式英語
關鍵詞brain iron; Cortex; Hepcidin; Hippocampus; Iron-overloaded rat; Reactive oxygen species (ROS); Striatum; Substantia nigra
Web of Science 學科類別Biochemistry & Molecular Biology; Endocrinology & Metabolism

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