Allyl isothiocyanate regulates caspase-1/receptor interacting protein-2 expression

被引:12
作者
Han, Na-Ra [1 ]
Park, Wansu [2 ]
Um, Jae-Young [1 ]
Kim, Hyung-Min [1 ]
Jeong, Hyun-Ja [3 ]
机构
[1] Kyung Hee Univ, Coll Oriental Med, Dept Pharmacol, Seoul 130701, South Korea
[2] Kyungwon Univ, Coll Oriental Med, Songnam 461701, South Korea
[3] Hoseo Univ, Biochip Res Ctr, Asan 336795, Chungnam, South Korea
关键词
Allyl isothiocyanate; Human mast cells; Calcium; Caspase-1; Receptor interacting proteins-2; Interleukin-1; beta; KAPPA-B ACTIVATION; MAST-CELLS; RELEASE; INTERLEUKIN-1-BETA; RIP2; LIPOPOLYSACCHARIDE; MACROPHAGES; SUPPRESSION; INHIBITION; APOPTOSIS;
D O I
10.1016/j.intimp.2010.12.021
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Isothiocyanates can inhibit nuclear factor-kappaB (NF-kappaB) activation. Interleukin (IL)-1 beta activates the NF-kappaB, which in turn activates proteins involved in inflammation. IL-1 beta is directly associated with caspase-1 activation. We tested the anti-inflammatory effect of allyl isothiocyanate (AITC) in mast cells. AITC suppressed the intracellular calcium level in the phorbol myristate acetate (PMA) plus calcium ionophore A23187-stimulated human mast cell line. AITC decreased PMA plus A23187-induced cystein-aspartic acid protease (caspase)-1 activity. Particularly, AITC decreased PMA plus A23187-induced caspase-1/receptor interacting protein-2 expression as well as the mRNA expression and production of IL-1 beta. An in-depth research of the cellular targets of the AITC is warranted. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:525 / 528
页数:4
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