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6-shogaol attenuates H2O2-induced oxidative stress via upregulation of Nrf2-mediated γ-glutamylcysteine synthetase and heme oxygenase expression in HepG2 cells
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  • 作者:Jin-Kyoung Kim ; Hae-Dong Jang
  • 关键词:6 ; shogaol ; oxidative stress ; c ; jun N ; terminal kinase ; mediated ; γ ; glutamylcysteine synthetase ; heme oxygenase ; 1
  • 刊名:Food Science and Biotechnology
  • 出版年:2016
  • 出版时间:February 2016
  • 年:2016
  • 卷:25
  • 期:1
  • 页码:319-327
  • 全文大小:629 KB
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  • 作者单位:Jin-Kyoung Kim (1)
    Hae-Dong Jang (1)

    1. Department of Food and Nutrition, Hannam University, Daejeon, 34054, Korea
  • 刊物类别:Chemistry and Materials Science
  • 刊物主题:Chemistry
    Nutrition
    Food Science
  • 出版者:The Korean Society of Food Science and Technology in co-publication with Springer
  • ISSN:2092-6456
文摘
The signaling pathway by which 6-shogaol protects HepG2 cells against H2O2-induced oxidative stress was investigated. Cellular anti-oxidant activities, the GSH level, and anti-oxidant response element (ARE) promoter activity were analyzed. Activated protein kinases and nuclear transcription factor-erythroid 2-related factor 2 (Nrf2) accumulation in the nucleus, and phase II detoxification and anti-oxidant enzymes were analyzed using western blotting. 6-Shogaol enhanced cellular anti-oxidant activities, the GSH level, and ARE promoter activities. Nrf2 accumulation in the nucleus, c-jun N-terminal kinase (JNK) activation, and γ-glutamylcysteine synthetase (GCS) and heme oxygenase-1 (HO-1) expressions were increased by 6-shogaol. Blockage of the JNK signaling pathway removed the elicitation effect of 6-shogaol on JNK activation, Nrf2 accumulation in nucleus, and GCS and HO-1 expression, but partially suppressed cellular anti-oxidant activities and ARE promoter activities. 6-shogaol exerts an indirect cellular anti-oxidant activity based on up-regulation of GCS and HO-1 via a JNK-mediated Nrf2 signaling pathway.

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