Kim Jin-Kyoung, Jang Hae-Dong
Department of Food and Nutrition, Hannam University, Daejeon, 34054 Korea.
Food Sci Biotechnol. 2016 Feb 29;25(1):319-327. doi: 10.1007/s10068-016-0045-3. eCollection 2016.
The signaling pathway by which 6-shogaol protects HepG2 cells against HO-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 -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.
研究了6-姜辣素保护HepG2细胞免受HO诱导的氧化应激的信号通路。分析了细胞抗氧化活性、谷胱甘肽（GSH）水平和抗氧化反应元件（ARE）启动子活性。使用蛋白质免疫印迹法分析了活化的蛋白激酶、核转录因子-红系2相关因子2（Nrf2）在细胞核中的积累以及II相解毒和抗氧化酶。6-姜辣素增强了细胞抗氧化活性、GSH水平和ARE启动子活性。6-姜辣素增加了Nrf2在细胞核中的积累、c-Jun末端激酶（JNK）的激活以及γ-谷氨酰半胱氨酸合成酶（GCS）和血红素加氧酶-1（HO-1）的表达。JNK信号通路的阻断消除了6-姜辣素对JNK激活、Nrf2在细胞核中的积累以及GCS和HO-1表达的诱导作用，但部分抑制了细胞抗氧化活性和ARE启动子活性。6-姜辣素通过JNK介导的Nrf2信号通路上调GCS和HO-1，从而发挥间接的细胞抗氧化活性。
