Benzyl isothiocyanate attenuates the hydrogen peroxide-induced interleukin-13 expression through glutathione S-transferase P induction in T lymphocytic leukemia cells.
Yue TangSho NaitoNaomi Abe-KanohSeiji OgawaShu YamaguchiBeiwei ZhuYoshiyuki MurataYoshimasa NakamuraPublished in: Journal of biochemical and molecular toxicology (2018)
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.
Keyphrases
- hydrogen peroxide
- induced apoptosis
- oxidative stress
- poor prognosis
- nitric oxide
- diabetic rats
- gene expression
- signaling pathway
- cell cycle arrest
- endoplasmic reticulum stress
- high glucose
- acute myeloid leukemia
- bone marrow
- cell death
- dna methylation
- cell proliferation
- long non coding rna
- protein kinase
- binding protein
- tyrosine kinase
- endothelial cells
- immune response
- mass spectrometry
- heat shock protein