國家衛生研究院 NHRI:Item 3990099045/9216
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    题名: Novel Nrf2/ARE activator, trans-coniferylaldehyde, induces a HO-1-mediated defense mechanism through a dual p38alpha/MAPKAPK-2 and PK-N3 signaling pathway
    其它题名: Novel Nrf2/ARE activator, trans-coniferylaldehyde, induces a HO-1-mediated defense mechanism through a dual p38α/MAPKAPK-2 and PK-N3 signaling pathway
    作者: Chen, HH;Wang, TC;Lee, YC;Shen, PT;Chang, JY;Yeh, TK;Huang, CH;Chang, HH;Cheng, SY;Lin, CY;Shih, C;Chen, CT;Liu, WM;Chen, CH;Kuo, CC
    贡献者: Institute of Biotechnology and Pharmaceutical Research;National Institute of Cancer Research
    摘要: The induction of detoxifying enzymes and antioxidant proteins by chemopreventive agents protects cells from oxidizing substances capable of damaging DNA integrity and initiating carcinogenesis. Coniferyl aldehyde, a naturally occurring substance, has been found in many foods and edible plants. We and others previously demonstrated that trans-coniferylaldehyde (t-CA) has potential antimutagenic and antioxidant properties. However, the mechanism underlying its Nrf2-mediated antioxidant effect remains largely unknown. In the present study, we demonstrated that t-CA significantly stimulated antioxidant-responsive element (ARE)-driven luciferase activity in a cell model and increased the expression of ARE-dependent detoxifying/antioxidant genes and their protein products in vitro and in vivo. The detoxifying/antioxidant genes activated by t-CA, especially heme oxygenase-1 (HO-1), were found to be involved in its cytoprotective effects against oxidative stress and cell injuries elicited by carcinogens tert-butylhydroperoxide and arecoline. Furthermore, the t-CA-induced phosphorylation and nuclear translocation of nuclear factor erythroid-2-related factor 2 (Nrf2) played a crucial role in this ARE-mediated cellular defense. Moreover, we found that p38 MAPK and protein kinase C (PKC) signaling pathways participated in the t-CA-induced, Nrf2-mediated cytoprotective effect. Among them, p38alpha/MAPKAPK-2 and an atypical PKC, PK-N3, were critical for the activation of the Nrf2/HO-1 axis by t-CA. In conclusion, we demonstrated for the first time that t-CA attenuates carcinogen-induced oxidative stress by activating Nrf2 via p38alpha/MAPKAPK-2- and PK-N3-dependent signaling pathways. In addition, t-CA increased the level of Nrf2-mediated detoxifying/antioxidant proteins in vivo, suggesting that t-CA may have potential for use in the management of carcinogenesis and meriting further investigation.
    日期: 2015-08
    關聯: Chemical Research in Toxicology. 2015 Aug ;28(9):1681-1692.
    Link to: http://dx.doi.org/10.1021/acs.chemrestox.5b00085
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0893-228X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000361865300005
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84941884870
    显示于类别:[郭靜娟] 期刊論文
    [陳炯東] 期刊論文
    [石全(2014-2017)] 期刊論文
    [葉燈光] 期刊論文
    [張俊彥] 期刊論文

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