Synergy between sulforaphane and selenium in protection against oxidative damage in colonic CCD841 cells

Yichong Wang, Christopher Dacosta, Wei Wang, Zhigang Zhou, Chun-Ming Liu, Yongping Bao

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Abstract

Dietary isothiocyanates (ITCs) are potent inducers of the NF-E2-related factor-2 (Nrf2) pathway. Sulforaphane (SFN), a representative ITC, has previously been shown to upregulate antioxidant enzymes such as selenium (Se) dependent thioredoxin reductase-1 (TrxR-1) in many tumour cell lines. In the present study, we hypothesized that a combination of SFN and Se would have a synergistic effect on the upregulation of TrxR-1 and the protection against oxidative damage in the normal colonic cell line CCD841. Treatment of cells with SFN and Se significantly induced TrxR-1 expression. Pre-treatment of cells with SFN protects against H2O2-induced cell death; this protection was enhanced by co-treatment with Se. The siRNA knockdown of either TrxR-1 or Nrf2 reduced the protection afforded by SFN and Se co-treatment; TrxR-1 and Nrf2 knockdown reduced cell viabilities to 66.5 and 51.1% respectively, down from 82.4% in transfection negative controls. This suggests that both TrxR-1 and Nrf2 are important in SFN-mediated protection against free radical-induced cell death. Moreover, flow cytometric analysis showed that TrxR-1 and Nrf2 were involved in SFN-mediated protection against H2O2-induced apoptosis. In summary, SFN activates the Nrf2 signaling pathway and protects against H2O2-mediated oxidative damage in normal colonic cells. Combined SFN and Se treatment resulted in a synergistic upregulation of TrxR-1 that in part contributed to the enhanced protection against free radical-mediated cell death provided by the co-treatment.
Original languageEnglish
Pages (from-to)610–617
Number of pages8
JournalNutrition Research
Volume35
Issue number7
Early online date30 May 2015
DOIs
Publication statusPublished - Jul 2015

Keywords

  • Cruciferous vegetable
  • sulforaphane
  • Selenium
  • Thioredoxin reductase
  • Nrf2
  • Colon cancer

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