Benzyl isothiocyanate attenuates the hydrogen peroxide-induced interleukin-13 expression through glutathione S-transferase P induction in T lymphocytic leukemia cells

Benzyl isothiocyanate attenuates the hydrogen peroxide-induced interleukin-13 expression through glutathione S-transferase P induction in T lymphocytic leukemia cells
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异硫氰酸苄酯通过谷胱甘肽 S-转移酶 P 诱导 T 淋巴细胞白血病细胞减弱过氧化氢诱导的白细胞介素 13 表达

DOI:
10.1002/jbt.22054
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发表时间:
2018
影响因子:
3.6
通讯作者:
Nakamura Yoshimasa
Nakamura Yoshimasa
中科院分区:
医学4区
文献类型:
--
作者:
Tang Yue;Naito Sho;Abe-Kanoh Naomi;Ogawa Seiji;Yamaguchi Shu;Zhu Beiwei;Murata Yoshiyuki;Nakamura Yoshimasa

文献摘要

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我们研究了异硫氰酸苄酯(BITC)对过氧化氢诱导的T淋巴细胞白血病Jurkat细胞中T辅助细胞因子白细胞介素(IL)-13基因表达的影响。BITC预处理24 h显著抑制过氧化氢增强的IL-13表达。虽然BITC预处理没有改变磷酸化c-Jun N-末端激酶(JNK)的增强水平,但它显著抑制过氧化氢诱导的c-Jun核转位。BITC还增加了谷胱甘肽S-转移酶(GST)同工酶,GST 1/2的蛋白表达,以及总GST活性。GST 1/2特异性抑制剂6-(7-硝基-2,1,3-苯并恶二唑-4-基硫基)己醇(NBDHEX)显著抵消了BITC对过氧化氢增强的IL-13上调以及c-Jun核转位的抑制作用。综上所述,这些结果表明,BITC抑制氧化应激介导的IL-13 mRNA表达,可能是通过GSTP干扰c-Jun磷酸化。
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 glutathioneS‐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.