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Int J Mol Med. 2016 Sep;38(3):912-8. doi: 10.3892/ijmm.2016.2667. Epub 2016 Jul 6.

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

Author information

1
Department of Molecular Microbiology and Immunology, Warren Alpert School of Medicine, Providence, RI 02912, USA.
2
National Marine Biodiversity Institute of Korea, Seocheon, Republic of Korea.
3
Department of Biomedical Engineering, and Center for Marine-Integrated Biomedical Technology (BK21 Plus), Pukyong National University, Busan, Republic of Korea.
4
Department of Biochemistry, College of Oriental Medicine, Dongeui University, Busan, Republic of Korea.
5
Department of Microbiology and Immunology, College of Medicine, Inje University, Busan, Republic of Korea.
6
Department of Internal Medicine, Busan Paik Hospital, College of Medicine, Inje University, Busan, Republic of Korea.
7
Department of Physiology, Kangwon National University School of Medicine, Chuncheon, Republic of Korea.

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.

PMID:
27430883
DOI:
10.3892/ijmm.2016.2667
[Indexed for MEDLINE]

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