Open Access

Allyl isothiocyanate increases MRP1 expression in cigarette smoke extract‑stimulated human bronchial epithelial cells via the JNK/Nrf2 pathway

  • Authors:
    • Min Zhang
    • Shujun Wang
    • Xueqi Wang
    • Xiaoya Xu
    • Zhaomin Yao
    • Wei Fang
    • Jie Wu
    • Qingqing Wu
    • Zegeng Li
    • Dianlei Wang
  • View Affiliations

  • Published online on: February 25, 2021     https://doi.org/10.3892/etm.2021.9840
  • Article Number: 409
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Multidrug resistance‑related protein 1 (MRP1) is involved in the biological transport of several molecules with diverse structural characteristics outside of the cell. In addition to its transport activity, MRP1 exhibits multiple defense mechanisms in vivo. MRP1 is highly expressed in normal lung tissues and plays a protective role in the process of chronic obstructive pulmonary disease. In the present study, human bronchial epithelial cells (16HBE14o‑cells) were stimulated by cigarette smoke extract (CSE) in vitro to simulate a smoking environment. On this basis, the mechanism of Allyl isothiocyanate (AITC) administration on the expression of MRP1 in CSE‑stimulated 16HBE14o‑cells was investigated. The effects of CSE on the viability of 16 HBE14o‑cells were investigated by an MTT assay. The changes in the mRNA expression levels of nuclear erythroid factor 2 (Nrf2) and MRP1 were investigated in CSE‑stimulated 16HBE14o‑cells using western blotting and reverse transcription quantitative PCR (RT‑qPCR). Immunofluorescence analysis was used to detect Nrf2 nuclear translocation. Incubation of the cells with 5% CSE for 24 h had minor effects on cell viability and resulted in the activation of the JNK and p38MAPK signaling pathways. AITC activated the JNK pathway, inhibited the activation of the p38MAPK pathway in 16HBE14o‑cells stimulated by 5% CSE and upregulated the expression levels of Nrf2 and MRP1 in a time‑dependent manner. The upregulation of Nrf2, MRP1 and of Nrf2, and MRP1 mRNA expression levels in CSE‑stimulated cells was inhibited by pretreatment with SP600125 (a JNK pathway inhibitor). Furthermore, the fluorescence intensity in the nucleus was significantly enhanced following AITC pretreatment and the analysis indicated nuclear translocation of Nrf2 in the cells. These results indicated that Nrf2 and MRP1 expression levels in CSE‑stimulated cells were altered following AITC pretreatment. Thus demonstrating that the primary mechanism may be associated with activation of the JNK pathway, while the p38MAPK pathway may not be involved.
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April-2021
Volume 21 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Zhang M, Wang S, Wang X, Xu X, Yao Z, Fang W, Wu J, Wu Q, Li Z, Wang D, Wang D, et al: Allyl isothiocyanate increases MRP1 expression in cigarette smoke extract‑stimulated human bronchial epithelial cells via the JNK/Nrf2 pathway. Exp Ther Med 21: 409, 2021
APA
Zhang, M., Wang, S., Wang, X., Xu, X., Yao, Z., Fang, W. ... Wang, D. (2021). Allyl isothiocyanate increases MRP1 expression in cigarette smoke extract‑stimulated human bronchial epithelial cells via the JNK/Nrf2 pathway. Experimental and Therapeutic Medicine, 21, 409. https://doi.org/10.3892/etm.2021.9840
MLA
Zhang, M., Wang, S., Wang, X., Xu, X., Yao, Z., Fang, W., Wu, J., Wu, Q., Li, Z., Wang, D."Allyl isothiocyanate increases MRP1 expression in cigarette smoke extract‑stimulated human bronchial epithelial cells via the JNK/Nrf2 pathway". Experimental and Therapeutic Medicine 21.4 (2021): 409.
Chicago
Zhang, M., Wang, S., Wang, X., Xu, X., Yao, Z., Fang, W., Wu, J., Wu, Q., Li, Z., Wang, D."Allyl isothiocyanate increases MRP1 expression in cigarette smoke extract‑stimulated human bronchial epithelial cells via the JNK/Nrf2 pathway". Experimental and Therapeutic Medicine 21, no. 4 (2021): 409. https://doi.org/10.3892/etm.2021.9840