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Benzyl isothiocyanate attenuates the hydrogen peroxide‐induced interleukin‐13 expression through glutathione S‐transferase P induction in T lymphocytic leukemia cells
Author(s) -
Tang Yue,
Naito Sho,
AbeKanoh Naomi,
Ogawa Seiji,
Yamaguchi Shu,
Zhu Beiwei,
Murata Yoshiyuki,
Nakamura Yoshimasa
Publication year - 2018
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22054
Subject(s) - chemistry , microbiology and biotechnology , glutathione , jurkat cells , benzyl isothiocyanate , hydrogen peroxide , fluorescein isothiocyanate , biochemistry , isothiocyanate , t cell , biology , enzyme , immunology , physics , immune system , quantum mechanics , fluorescence
We investigated the effect of benzyl isothiocyanate (BITC) on the hydrogen peroxide‐induced gene expression of a T‐helper‐2 cytokine, interleukin (IL)‐13, in T lymphocytic leukemia Jurkat cells. The 24‐h pretreatment of BITC significantly inhibited the IL‐13 expression enhanced by hydrogen peroxide. Although the BITC pretreatment did not change the enhanced level of the phosphorylated c‐Jun N‐terminal kinase (JNK), it significantly inhibited the nuclear translocation of c‐Jun induced by hydrogen peroxide. BITC also increased the protein expression of glutathione S ‐transferase (GST) isozymes, GSTP1/2, as well as the total GST activity. A GSTP1/2‐specific inhibitor, 6‐(7‐nitro‐2,1,3‐benzoxadiazol‐4‐ylthio)hexanol (NBDHEX), significantly counteracted the inhibitory effect of BITC on the hydrogen peroxide‐enhanced IL‐13 upregulation as well as the c‐Jun nuclear translocation. Taken together, these results suggested that BITC inhibits the oxidative stress‐mediated IL‐13 mRNA expression, possibly through interference of the c‐Jun phosphorylation by GSTP.