Role of the nrf-2 gene in protection and repair of gastric mucosa against oxidative stress

被引：29
作者：
Yanaka A. [1 ,2 ]
Zhang S. [1 ,2 ]
Tauchi M. [1 ,2 ]
Suzuki H. [1 ,2 ]
Shibahara T. [1 ,2 ]
Matsui H. [1 ,2 ]
Nakahara A. [1 ,2 ]
Tanaka N. [1 ,2 ]
Yamamoto M. [3 ]
机构：
[1] Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575
[2] Department of Endoscopy, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575
[3] Center for Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Tsukuba, Ibaraki 305-8575
来源：
InflammoPharmacology | 2005年 / 13卷 / 1-3期
关键词：
Anti-oxidant; Free radical; Knockout mice; Sulforaphane; Ussing chamber;
D O I：
10.1163/156856005774423863
中图分类号：
学科分类号：
摘要：
Helicobacter pylori infection, as well as NSAIDs induce oxidative stress on gastric mucosa, thereby causing mucosal damage and retarding mucosal repair. Cells can survive against chronic oxidative stress by enhancing activities of anti-oxidant enzymes, thereby protecting cells from DNA damage. Recent studies have clearly shown that the gene encoding Nrf-2 (NF-E2 p45-related factor-2) plays an important role in the induction of antioxidant enzymes against oxidative stress. In this paper, we will describe the cellular mechanisms by which the nrf-2 gene stimulates anti-oxidant enzyme activities during exposure to oxidative stress. Secondly, we will also mention the beneficial effects of sulforaphane, an isothiocyanate family which is abundantly included in broccoli sprouts, on gastric mucosa. Sulforaphane stimulates nrf-2 gene-dependent anti-oxidant enzyme activities, thereby protecting cells from oxidative injury. Finally, we will state our perspective on the efficacy of sulforaphane in protection and repair of gastric mucosa against oxidative stress during H. pylori infection. © VSP 2005.
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页码：83 / 90
页数：7
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