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KMID : 1007520160250010319
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Food Science and Biotechnology
2016 Volume.25 No. 1 p.319 ~ p.327
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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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Kim Jin-Kyoung
Jang Hae-Dong
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Abstract
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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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KEYWORD
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6-shogaol, oxidative stress, c-jun N-terminal kinase-mediated, γ-glutamylcysteine synthetase, heme oxygenase-1
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