Dietz Birgit M, Kang Young-Hwa, Liu Guowen, Eggler Aimee L, Yao Ping, Chadwick Lucas R, Pauli Guido F, Farnsworth Norman R, Mesecar Andrew D, van Breemen Richard B, Bolton Judy L
Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago, 833 South Wood Street, M/C 781, Chicago, Illinois 60612-7231, USA.
Chem Res Toxicol. 2005 Aug;18(8):1296-305. doi: 10.1021/tx050058x.
The female parts of hops (Humulus lupulus L.) show estrogenic effects as well as cancer chemopreventive potential. We analyzed the chemopreventive mechanism of hops by studying its antioxidative activities and its effect on the detoxification of a potentially toxic quinone (menadione). The detoxification enzyme quinone reductase [(NAD(P)H:quinone oxidoreductase, QR] protects against quinone-induced toxicity and has been used as a marker in cancer chemoprevention studies. Although the hop extract was only a weak quencher of free radicals formed from 1,1-diphenyl-2-picrylhydrazyl, it demonstrated strong QR induction in Hepa 1c1c7 cells. In addition, compounds isolated from hops including xanthohumol (XH) and 8-prenylnaringenin were tested for QR induction. Among these, XH was the most effective at inducing QR with a concentration required to double the specific activity of QR (CD value) of 1.7 +/- 0.7 microM. In addition, pretreatment of Hepa1c1c7 cells with XH significantly inhibited menadione-induced DNA single-strand breaks. The QR inhibitor dicumarol reversed the protective effect of XH against menadione-induced DNA damage. Because the expression of QR and other detoxifying enzymes is known to be upregulated by binding of the transcription factor Nrf2 to the antioxidant response element (ARE), the reporter activity mediated by ARE in HepG2-ARE-C8 cells was investigated after incubation with XH for 24 h. Under these conditions, XH increased ARE reporter activity in a dose-dependent manner. One mechanism by which XH might induce QR could be through interaction with Keap1, which sequesters Nrf2 in the cytoplasm, so that it cannot activate the ARE. Using LC-MS-MS, we demonstrated that XH alkylates human Keap1 protein, most likely on a subset of the 27 cysteines of Keap1. This suggests that XH induces QR by covalently modifying the Keap1 protein. Therefore, XH and hops dietary supplements might function as chemopreventive agents, through induction of detoxification enzymes such as QR.
啤酒花(Humulus lupulus L.)的雌性部分具有雌激素效应以及癌症化学预防潜力。我们通过研究啤酒花的抗氧化活性及其对潜在有毒醌(甲萘醌)解毒作用的影响,分析了啤酒花的化学预防机制。解毒酶醌还原酶[(NAD(P)H:醌氧化还原酶,QR]可预防醌诱导的毒性,并已在癌症化学预防研究中用作标志物。尽管啤酒花提取物只是1,1 - 二苯基 - 2 - 苦基肼自由基的弱猝灭剂,但它在Hepa 1c1c7细胞中表现出强烈的QR诱导作用。此外,对从啤酒花中分离出的化合物,包括黄腐酚(XH)和8 - 异戊烯基柚皮素进行了QR诱导测试。其中,XH诱导QR的效果最为显著,使QR比活性加倍所需的浓度(CD值)为1.7±0.7 microM。此外,用XH预处理Hepa1c1c7细胞可显著抑制甲萘醌诱导的DNA单链断裂。QR抑制剂双香豆素可逆转XH对甲萘醌诱导的DNA损伤的保护作用。由于已知转录因子Nrf2与抗氧化反应元件(ARE)结合可上调QR和其他解毒酶的表达,因此在与XH孵育24小时后,研究了HepG2 - ARE - C8细胞中ARE介导的报告基因活性。在这些条件下,XH以剂量依赖的方式增加ARE报告基因活性。XH诱导QR的一种机制可能是通过与Keap1相互作用,Keap1将Nrf2隔离在细胞质中,使其无法激活ARE。使用液相色谱 - 串联质谱法(LC - MS - MS),我们证明XH使人类Keap1蛋白烷基化,最有可能是在Keap1的27个半胱氨酸的一个子集中。这表明XH通过共价修饰Keap1蛋白来诱导QR。因此,XH和啤酒花膳食补充剂可能通过诱导QR等解毒酶发挥化学预防剂的作用。