Detoxifying effect of fermented black ginseng on H2O2-induced oxidative stress in HepG2 cells

Detoxifying effect of fermented black ginseng on H2O2-induced oxidative stress in HepG2 cells
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DOI:
10.3892/ijmm.2014.1972
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发表时间:
2014-12-01
影响因子:
5.4
通讯作者:
Kim, Kyu-Bong
Kim, Kyu-Bong
中科院分区:
医学3区
文献类型:
--
作者:
Bak, Min-Ji;Jeong, Woo-Sik;Kim, Kyu-Bong

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发酵黑参(FBG)是用新鲜人参经过反复蒸煮和干燥过程,然后用酿酒酵母发酵而制成的。最近显示它具有多种生物活性。 FBG含有粗皂苷(1,440μg/ml)、人参皂苷Rg2(2.86μg/ml)、人参皂苷Rg3(24.52μg/ml)、人参皂苷Rh1(12.64μg/ml)、人参皂苷Rh2(0.63μg/ml)和人参皂苷Rf(1.32μg/ml) 克/毫升)。本研究调查了 FBG 对 HepG2 人肝细胞癌细胞中过氧化氢 (H2O2) 介导的氧化应激的抗氧化防御特性。当细胞用 FBG (10-50 μg/ml) 预处理时,H2O2 诱导的活性氧 (ROS) 产生的增加以剂量依赖性方式减弱。 FBG 诱导 H2O2 处理的 HepG2 细胞中抗氧化酶的表达和活性,例如超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶。还观察到 FBG 对上游丝裂原激活蛋白激酶 (MAPK) 磷酸化的抑制作用,例如 c-Jun N 末端激酶、细胞外信号调节激酶和 p38。总的来说,我们的结果表明,FBG 通过诱导抗氧化酶活性和抑制 MA PK 途径,保护 HepG2 细胞免受氧化应激。
Fermented black ginseng (FBG) is prepared by repeated steaming and drying processes with fresh ginseng followed by fermentation with Saccharomyces cerevisiae. It has recently been shown to have several bioactivities. FBG contains crude saponin (1,440 mu g/ml) ginsenoside Rg2 (2.86 mu g/ml), ginsenoside Rg3 (24.52 mu g/ml), ginsenoside Rh1 (12.64 mu g/ml), ginsenoside Rh2 (0.63 mu g/ml) and ginsenoside Rf (1.32 mu g/ml). The present study investigated the antioxidant defense properties of FBG against hydrogen peroxide (H2O2)-mediated oxidative stress in HepG2 human hepatocellular carcinoma cells. The increased production of reactive oxygen species (ROS) induced by H2O2 was attenuated in a dose-dependent manner when the cells were pre-treated with FBG (10-50 mu g/ml). FBG induced both the expression and activity of antioxidant enzymes, such as superoxide dismutase, catalase and glutathione peroxidase in the H2O2-treated HepG2 cells. The inhibitory effects of FBG on the phosphorylation of upstream mitogen-activated protein kinases (MAPKs), such as c-Jun N-terminal kinase, extracellular signal-regulated kinase and p38 were also observed. Overall, our results demonstrate that FBG protects HepG2 cells from oxidative stress through the induction of antioxidant enzyme activity and the inhibition of MA PK pathways.