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首页> 外文期刊>Mediators of inflammation >alpha-Lipoic Acid Inhibits Helicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells
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alpha-Lipoic Acid Inhibits Helicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells

机译：α-硫辛酸通过抑制胃上皮细胞中NADPH氧化酶的活化来抑制幽门螺杆菌诱导的癌基因表达和过度增殖

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摘要

Hyperproliferation and oncogene expression are observed in the mucosa of Helicobacter pylori- (H. pylori-) infected patients with gastritis or adenocarcinoma. Expression of oncogenes such as beta-catenin and c-myc is related to oxidative stress. a-Lipoic acid (a-LA), a naturally occurring thiol compound, acts as an antioxidant and has an anticancer effect. The aim of this study is to investigate the effect of a-LA on H. pylori-induced hyperproliferation and oncogene expression in gastric epithelial AGS cells by determining cell proliferation (viable cell numbers, thymidine incorporation), levels of reactive oxygen species (ROS), NADPH oxidase activation (enzyme activity, subcellular levels of NADPH oxidase subunits), activation of redox-sensitive transcription factors (NF-kB, AP-1), expression of oncogenes (beta-catenin, c-myc), and nuclear localization of /?-catenin. Furthermore, we examined whether NADPH oxidase mediates oncogene expression and hyperproliferation in H. pylori-infected AGS cells using treatment of diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase. As a result, a-LA inhibited the activation of NADPH oxidase and, thus, reduced ROS production, resulting in inhibition on activation of NF-kB and AP-1, induction of oncogenes, nuclear translocation of beta-catenin, and hyperproliferation in H. pylori-infected AGS cells. DPI inhibited H. pylori-induced activation of NF-kB and AP-1, oncogene expression and hyperproliferation by reducing ROS levels in AGS cells. In conclusion, we propose that inhibiting NADPH oxidase by a-LA could prevent oncogene expression and hyperproliferation occurring in H. pylori-infected gastric epithelial cells.
机译：在幽门螺杆菌（H. Pylori-）感染胃炎患者的胃炎或腺癌患者的粘膜中观察到过增殖和癌基因表达。诱导腺苷酸和C-MYC等癌素的表达与氧化应激有关。 A-硫辛酸（A-LA）是天然存在的硫醇化合物，作为抗氧化剂并具有抗癌效果。本研究的目的是通过确定细胞增殖（活细胞数，胸苷掺入），反应性氧（ROS）水平来研究A-LA对H.幽门螺杆菌诱导的高增殖和癌基因表达的影响。 ，NADPH氧化酶活化（酶活性，NADPH氧化酶亚基的亚细胞水​​平），氧化还原敏感性转录因子的激活（NF-KB，AP-1），癌基因的表达（β-连环蛋白，C-MYC）和核定位/？ - catenin。此外，我们研究了NADPH氧化酶是否使用丁基碘碘鎓（DPI），NADPH氧化酶的抑制剂介导幽门螺杆菌感染的AGS细胞中的甲基植物感染的AGS细胞。结果，A-LA抑制了NADPH氧化酶的活化，从而减少了ROS生产，导致NF-KB和AP-1的活化抑制，诱导癌素，β-连环蛋白的诱导，H中的高增殖。幽门螺杆菌感染的AGS细胞。通过降低AGS细胞中的ROS水平，DPI抑制幽门螺杆菌诱导的NF-KB和AP-1，癌基因表达和过度增殖的活化。总之，我们提出抑制A-LA的NAD​​PH氧化酶可以预防幽门螺杆菌感染胃上皮细胞中的癌基因表达和高增殖。

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  • 来源
    《Mediators of inflammation》 |2014年第6期|共1页
  • 作者

    Eunyoung Byun;

  • 作者单位

    Department of Food and Nutrition Brain Korea 21 PLUS Project College of Human Ecology Yonsei;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 病理学;
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