Dimethyl sulfoxide inhibits NLRP3 inflammasome activation

被引:67
作者
Ahn, Huijeong [1 ,2 ]
Kim, Jeeyoung [1 ,2 ]
Jeung, Eui-Bae [3 ]
Lee, Geun-Shik [1 ,2 ]
机构
[1] Kangwon Natl Univ, Coll Vet Med, Chunchon 200701, Gangwon, South Korea
[2] Kangwon Natl Univ, Inst Vet Sci, Chunchon 200701, Gangwon, South Korea
[3] Chungbuk Natl Univ, Coll Vet Med, Lab Vet Biochem & Mol Biol, Cheongju 361763, South Korea
基金
新加坡国家研究基金会;
关键词
Cytokine; DMSO; Inflammasome; Interleukin-1; Macrophages; NLRP3; SCAVENGER RECEPTOR; NALP3; INFLAMMASOME; EXPRESSION; IL-1-BETA; DMSO; TYPHIMURIUM; MACROPHAGES; INVASION; FAMILY; CELLS;
D O I
10.1016/j.imbio.2013.11.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Dimethyl sulfoxide (DMSO) is an amphipathic molecule that is commonly/widely used as a solvent for biological compounds. In addition, DMSO has been studied as a medication for the treatment of inflammation, cystitis, and arthritis. Based on the anti-inflammatory characteristics of DMSO, we elucidated the effects of DMSO on activation of inflammasomes, which are cytoplasmic multi-protein complexes that mediate the maturation of interleukin (IL)-1 beta by activating caspase-1 (Caspl). In the present study, we prove that DMSO attenuated IL-1 beta maturation, Caspl activity, and ASC pyroptosome formation via NLRP3 inflammasome activators. Further, NLRC4 and AIM2 inflammasome activity were not affected, suggesting that DMSO is a selective inhibitor of the NLRP3 inflammasomes. The anti-inflammatory effect of DMSO was further confirmed in animal, LPS-endotoxin sepsis and inflammatory bowel disease models. In addition, DMSO inhibited LPS-mediating IL-1s transcription. Taken together, DMSO shows anti-inflammatory characteristics, attenuates NLRP3 inflammasome activation, and mediates inhibition of IL-1s transcription. Crown Copyright (C) 2013 Published by Elsevier GmbH. All rights reserved.
引用
收藏
页码:315 / 322
页数:8
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