Protective effect of sulforaphane on indomethacin-induced cytotoxicity via heme oxygenase-1expression in human intestinal Int 407 cells

Chi Tai Yeh, Hsiang Fan Chiu, Gow Chin Yen

研究成果: 雜誌貢獻文章

25 引文 (Scopus)

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.
原文英語
頁(從 - 到)1166-1176
頁數11
期刊Molecular Nutrition and Food Research
53
發行號9
DOIs
出版狀態已發佈 - 2009
對外發佈Yes

指紋

heme oxygenase (biliverdin-producing)
Heme Oxygenase (Decyclizing)
indomethacin
heme
oxygenases
Indomethacin
protective effect
cytotoxicity
Heme Oxygenase-1
NF-E2-Related Factor 2
mitogen-activated protein kinase
cells
oxidative stress
antioxidants
protein synthesis inhibitors
consensus sequence
Oxidative Stress
nuclear proteins
Antioxidants
cycloheximide

ASJC Scopus subject areas

  • Food Science
  • Biotechnology

引用此文

Protective effect of sulforaphane on indomethacin-induced cytotoxicity via heme oxygenase-1expression in human intestinal Int 407 cells. / Yeh, Chi Tai; Chiu, Hsiang Fan; Yen, Gow Chin.

於: Molecular Nutrition and Food Research, 卷 53, 編號 9, 2009, p. 1166-1176.

研究成果: 雜誌貢獻文章

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abstract = "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.",
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AB - 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.

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