Abstract Title:

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

Abstract Source:

Int J Mol Med. 2016 Sep ;38(3):912-8. Epub 2016 Jul 6. PMID: 27430883

Abstract Author(s):

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

Article Affiliation:

Chang-Min Lee


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 regulateneuroinflammation through the inflammasome-mediated signaling pathway.

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