Cytoprotective effects of a tripeptide from Chinese Baijiu against AAPH-induced oxidative stress in HepG2 cells via Nrf2 signaling.
Cytoprotective effects of a tripeptide from Chinese Baijiu against AAPH-induced oxidative stress in HepG2 cells via Nrf2 signaling.
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中国白酒三肽通过 Nrf2 信号传导对 HepG2 细胞中 AAPH 诱导的氧化应激的细胞保护作用
DOI：
10.1039/c8ra01162a
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发表时间：
2018-03-16
期刊：
影响因子：
3.9
通讯作者：
Huang, Mingquan
中科院分区：
文献类型：
--
作者：
Wu, Jihong;Sun, Baoguo;Luo, Xuelian;Zhao, Mouming;Zheng, Fuping;Sun, Jinyuan;Li, Hehe;Sun, Xiaotao;Huang, Mingquan
抗氧化肽已被广泛报道，而我们从白酒中新分离鉴定的一种三肽（Pro-His-Pro， PHP）的细胞内抗氧化活性尚不清楚。本研究探讨了PHP对2,2 ' -偶氮（2-甲基-丙氨脒）二盐酸（AAPH）诱导的HepG2细胞氧化应激的保护作用及其分子机制。PHP预处理能抑制活性氧（ROS）、丙二醛（MDA）和氧化谷胱甘肽（GSSG）的生成，阻止还原性谷胱甘肽（GSH）的减少，上调细胞抗氧化酶的活性。此外，PHP刺激了抗氧化酶和核因子E2相关因子2 (Nrf2) mRNA和蛋白的表达水平。同时，PHP显著降低Kelch-like ECH-associated protein 1 （Keap1）水平，提示PHP有效激活Nrf2/抗氧化反应元件（anti - oxide response element， ARE）介导的活性。这些发现为PHP预防aaph诱导的氧化应激的健康促进作用提供了第一个分子基础。
Antioxidant peptides have been widely reported, whereas the intracellular antioxidant activity of a tripeptide (Pro-His-Pro, PHP), which was newly isolated and identified from Chinese Baijiu in our previous study, are still poorly understood. This study investigated the protective effects of PHP on 2,2′-azobis (2-methyl-propanimidamidine) dihydrochloride (AAPH)-induced oxidative stress in HepG2 cells and the involved molecular mechanisms. Pretreatment with PHP suppressed the generations of reactive oxygen species (ROS), malondialdehyde (MDA) and oxidized glutathione (GSSG), prevented a decrease in reduced glutathione (GSH), and up-regulated the activities of cellular antioxidant enzymes. Moreover, PHP treatment stimulated the mRNA and protein expression levels of antioxidant enzymes and nuclear factor E2 related factor 2 (Nrf2). Meanwhile, PHP markedly reduced the level of Kelch-like ECH-associated protein 1 (Keap1), suggesting that PHP effectively activated Nrf2/antioxidant response element (ARE)-mediated activity. These findings provide the first molecular basis for the health-promoting effects of PHP to prevent AAPH-induced oxidative stress.
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