Benzyl isothiocyanate inhibits inflammasome activation in E. coli LPS-stimulated BV2 cells

  • Authors:
    • Chang-Min Lee
    • Dae-Sung Lee
    • Won-Kyo Jung
    • Jong Su Yoo
    • Mi-Jin Yim
    • Yung Hyun Choi
    • Saegwang Park
    • Su-Kil Seo
    • Jung Sik Choi
    • Young-Min Lee
    • Won Sun Park
    • Il-Whan Choi
  • View Affiliations

  • Published online on: July 6, 2016     https://doi.org/10.3892/ijmm.2016.2667
  • Pages: 912-918
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Abstract

Inflammasomes are multi-protein complexes that play a crucial role in innate immune responses. Benzyl isothiocyanate (BITC) is a naturally occurring compound found in cruciferous vegetables, and BITC exhibits potential as a chemopreventive agent. However, whether BITC exerts inflammasome-mediated regulatory effects on neuroinflammation is unknown. In this study, we examined the effects of BITC on inflammasome-mediated interleukin-1β (IL-1β) production in E. coli lipopolysaccharide (LPS)-stimulated BV2 microglial cells. IL-1β production is tightly regulated at the post-translational level through the inflammasoume. We measured the levels of IL-1β produced from the LPS-exposed BV2 microglial cells using enzyme-linked immunosorbent assays (ELISAs). The BITC regulatory mechanisms in inflammasome-mediated cellular signaling pathways were examined by RT-PCR, western blot analysis and electrophoretic mobility shift assays. BITC inhibited the secretion of IL-1β induced by LPS in the BV2 microglial cells. BITC inhibited inflammasome activation and NLR family, pyrin domain containing 3 (NLRP3)-mediated caspase-1 activation, and decreased the levels of inflammasome activation pro-inflammatory mediators, including mitochondrial reactive oxygen species (ROS) and adenosine triphosphate (ATP) secretion in the LPS-stimulated BV2 microglial cells. Furthermore, we demonstrated that nuclear factor-κB (NF-κB) activation induced by LPS was inhibited by BITC, which may contribute to the attenuated secretion of IL-1β. These BITC-mediated inhibitory effects on IL-1β expression may thus regulate neuroinflammation through the inflammasome-mediated signaling pathway.
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September-2016
Volume 38 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Lee C, Lee D, Jung W, Yoo JS, Yim M, Choi YH, Park S, Seo S, Choi JS, Lee Y, Lee Y, et al: Benzyl isothiocyanate inhibits inflammasome activation in E. coli LPS-stimulated BV2 cells. Int J Mol Med 38: 912-918, 2016.
APA
Lee, C., Lee, D., Jung, W., Yoo, J.S., Yim, M., Choi, Y.H. ... Choi, I. (2016). Benzyl isothiocyanate inhibits inflammasome activation in E. coli LPS-stimulated BV2 cells. International Journal of Molecular Medicine, 38, 912-918. https://doi.org/10.3892/ijmm.2016.2667
MLA
Lee, C., Lee, D., Jung, W., Yoo, J. S., Yim, M., Choi, Y. H., Park, S., Seo, S., Choi, J. S., Lee, Y., Park, W. S., Choi, I."Benzyl isothiocyanate inhibits inflammasome activation in E. coli LPS-stimulated BV2 cells". International Journal of Molecular Medicine 38.3 (2016): 912-918.
Chicago
Lee, C., Lee, D., Jung, W., Yoo, J. S., Yim, M., Choi, Y. H., Park, S., Seo, S., Choi, J. S., Lee, Y., Park, W. S., Choi, I."Benzyl isothiocyanate inhibits inflammasome activation in E. coli LPS-stimulated BV2 cells". International Journal of Molecular Medicine 38, no. 3 (2016): 912-918. https://doi.org/10.3892/ijmm.2016.2667