國家衛生研究院 NHRI:Item 3990099045/3882
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    题名: Protective effect of sulforaphane on indomethacin-induced cytotoxicity via heme oxygenase-1 expression in human intestinal Int 407 cells
    作者: Yeh, CT;Chiu, HF;Yen, GC
    贡献者: National Institute of Cancer Research
    摘要: Sulforaphane is known to be an indirect antioxidant that acts by inducing NF-E2-related factor 2 (Nrf2)-dependent phase II enzymes. In the present study, we investigated the effect of sulforaphane on the expression of heme oxygenase-1 (HO-1) in human intestinal Int 407 cells. RT-PCR and West- ern blot data revealed that sulforaphane induced an increase in HO-1 expression at the mRNA and protein levels, respectively. This induction was also marked by an increase in HO-1 activity. Actino- mycin D (an RNA synthesis inhibitor) and cycloheximide (a protein synthesis inhibitor) inhibited sul- foraphane-responsive HO-1 mRNA expression, indicating that sulforaphane is a requirement for tran- scription and de novo protein synthesis. Moreover, sulforaphane increased the nuclear levels of Nrf2 and increased the binding activity of nuclear proteins to the antioxidant responsive element consensus sequence. We also found that U0126, an ERK kinase inhibitor, suppressed the sulforaphane-induced HO-1 expression and nuclear translocation of Nrf2. Moreover, the cytoprotective effect of sulfora- phane on indomethancin-induced cytotoxicity was partially blocked by ERK and HO-1 inhibitors, fur- ther demonstrating that sulforaphane attenuated oxidative stress through a pathway that involved ERK and HO-1. Taken together, this study gives additional support to the possible use of sulforaphane as a dietary preventive agent against oxidative stress-induced intestinal injury.
    日期: 2009-09
    關聯: Molecular Nutrition and Food Research. 2009 Sep;53(9):1166-1176.
    Link to: http://dx.doi.org/10.1002/mnfr.200800558
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1613-4125&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000270329600010
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=70349639202
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