Electrophilic and Reactive Oxygen Species Detoxification Potentials of Chalcone Dimers is Mediated by Redox Transcription Factor Nrf-2
Electrophilic and Reactive Oxygen Species Detoxification Potentials of Chalcone Dimers is Mediated by Redox Transcription Factor Nrf-2
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DOI：
10.1002/jbt.21517
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发表时间：
2014-01-01
影响因子：
3.6
通讯作者：
Oladiji, Adenike T.
中科院分区：
文献类型：
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作者：
Ajiboye, Taofeek O.;Yakubu, Musa T.;Oladiji, Adenike T.
核红细胞相关因子2（Nuclearerythroidrelatedfactor-2，Nrf 2）是一种氧化还原转录因子，在亲电子和活性氧的解毒中起着关键作用。这使其成为多酚调节的候选者。本研究探讨了查耳酮二聚体（洛非酮B和C）诱导细胞保护酶表达和活性的能力。查尔酮二聚体给药大鼠不仅诱导Nrf 2，但也抑制细胞质Kelch样ECH相关蛋白1（Keap 1）的表达。此外，查耳酮二聚体显著（p < 0.05）增加了大鼠肝脏中烟酰胺腺嘌呤二核苷酸的表达和活性，并降低了醌氧化还原酶-1、谷胱甘肽-S-转移酶、环氧化物水解酶和尿苷酰葡萄糖醛酸转移酶的活性。肝组织超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性显著升高（p < 0.05）。总体而言，洛非酮B和C可能通过降低细胞质Keap 1表达，导致Nrf 2核转位，从而增加大鼠肝脏中细胞保护蛋白的表达和活性。(C)2013 Wiley Periodicals，Inc.
Nuclear erythroid related factor-2 (Nrf2), a redox-transcription factor, plays a critical role in the detoxification of electrophilic and reactive oxygen species that halt various biochemical and molecular processes. This makes it a candidate for regulation by polyphenols. This study investigates the capability of chalcone dimers (lophirones B and C) to induce expressions and activities of cytoprotective enzymes. Chalcone dimers administration to rats not only induced the Nrf2, but also suppressed cytoplasmic Kelch-like ECH-associated protein 1 (Keap1) expressions. In addition, the chalcone dimers significantly (p < 0.05) increased the expressions and activities of nicotinamide adenine dinucleotide and reduced quinone oxidoreductase-1, glutathione-S-transferase, epoxide hydrolase and uridyl glucuronosyl transferase in rat liver. Also, activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase in rat liver increased significantly (p < 0.05). Overall, lophirones B and C increased the expressions and activities of cytoprotective proteins in rat liver possibly through the reduction of cytoplasmic Keap1 expression, leading to the nuclear translocation of Nrf2. (C) 2013 Wiley Periodicals, Inc.