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Inhibition of epithelial to mesenchymal transition in metastatic prostate cancer cells by the novel proteasome inhibitor, NPI-0052: pivotal roles of Snail repression and RKIP induction.新型蛋白酶体抑制剂NPI-0052对转移性前列腺癌细胞上皮-间质转化的抑制作用:Snail抑制和RKIP诱导的关键作用
Oncogene. 2009 Oct 8;28(40):3573-85. doi: 10.1038/onc.2009.214. Epub 2009 Jul 27.
2
Signals triggered by a bacterial pore-forming toxin contribute to toll-like receptor redundancy in gram-positive bacterial recognition.由细菌成孔毒素触发的信号有助于革兰氏阳性菌识别中的Toll样受体冗余。
J Infect Dis. 2009 Jan 1;199(1):124-33. doi: 10.1086/595562.
3
High mortality rate of (NZW x BXSB)F1 mice induced by administration of lipopolysaccharide attributes to high production of tumour necrosis factor-alpha by increased numbers of dendritic cells.给予脂多糖诱导的(新西兰白兔×BXSB)F1小鼠高死亡率归因于树突状细胞数量增加导致肿瘤坏死因子-α的高产量。
Clin Exp Immunol. 2008 Nov;154(2):285-93. doi: 10.1111/j.1365-2249.2008.03759.x. Epub 2008 Sep 8.
4
Inactivation of NF-kappaB components by covalent binding of (-)-dehydroxymethylepoxyquinomicin to specific cysteine residues.(-)-去氢甲基环氧喹喔啉霉素通过与特定半胱氨酸残基共价结合使NF-κB组分失活。
J Med Chem. 2008 Sep 25;51(18):5780-8. doi: 10.1021/jm8006245. Epub 2008 Aug 26.
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The novel NF-kappaB activation inhibitor dehydroxymethyl-epoxyquinomicin suppresses anti-Thy1.1-induced glomerulonephritis in rats.新型核因子κB激活抑制剂去羟甲基环氧醌霉素可抑制大鼠抗Thy1.1诱导的肾小球肾炎。
Nephron Exp Nephrol. 2008;110(1):e17-24. doi: 10.1159/000150314. Epub 2008 Aug 6.
6
Inhibition of inflammatory mediator secretion by (-)-DHMEQ in mouse bone marrow-derived macrophages.(-)-DHMEQ对小鼠骨髓来源巨噬细胞炎症介质分泌的抑制作用
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Effects of a novel NF-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on growth, apoptosis, gene expression, and chemosensitivity in head and neck squamous cell carcinoma cell lines.新型核因子-κB抑制剂去羟甲基环氧喹霉素(DHMEQ)对头颈部鳞状细胞癌细胞系生长、凋亡、基因表达及化疗敏感性的影响
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Effect of a small molecule inhibitor of nuclear factor-kappaB nuclear translocation in a murine model of arthritis and cultured human synovial cells.核因子-κB核易位小分子抑制剂在小鼠关节炎模型及培养的人滑膜细胞中的作用
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去甲氧基环氧米托蒽醌(DHMEQ)可抑制脂多糖诱导的小鼠肿瘤坏死因子-α的产生,从而使小鼠在体内免于死亡。

Dehydroxymethylepoxyquinomicin (DHMEQ) can suppress tumour necrosis factor-α production in lipopolysaccharide-injected mice, resulting in rescuing mice from death in vivo.

机构信息

Department of Pediatrics, Kansai Medical University, Moriguchi City, Osaka, Japan.

出版信息

Clin Exp Immunol. 2011 Nov;166(2):299-306. doi: 10.1111/j.1365-2249.2011.04475.x.

DOI:10.1111/j.1365-2249.2011.04475.x
PMID:21985376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3219905/
Abstract

Dehydroxymethylepoxyquinomicin (DHMEQ), a new nuclear factor (NF)-κB inhibitor, has several beneficial effects, including the suppression of tumour growth and anti-inflammatory effects. DHMEQ can also suppress the production of tumour necrosis factor (TNF)-α induced by lipopolysaccharide (LPS) in vitro. In the present study, we examine the effects of DHMEQ on TNF-α production in vivo and on the survival of mice injected with LPS. When DHMEQ was injected into mice 2 h before LPS injection, the survival of the LPS-injected mice was prolonged. When DHMEQ was injected twice (2 h before LPS injection and the day after LPS injection), all the mice were rescued. The injection of DHMEQ 1 h after LPS injection and the day after LPS injection also resulted in the rescue of all mice. The serum levels of TNF-α in the mice that received both LPS and DHMEQ were suppressed compared to the mice that received only LPS. These results suggest that DHMEQ can be utilized for the prevention and treatment of endotoxin shock.

摘要

去甲氧基环氧小檗碱(DHMEQ)是一种新型核因子(NF)-κB 抑制剂,具有多种有益作用,包括抑制肿瘤生长和抗炎作用。DHMEQ 还可以抑制脂多糖(LPS)体外诱导的肿瘤坏死因子(TNF)-α的产生。在本研究中,我们研究了 DHMEQ 对体内 TNF-α产生和 LPS 注射小鼠存活的影响。当 DHMEQ 在 LPS 注射前 2 小时注射到小鼠体内时,LPS 注射小鼠的存活时间延长。当 DHMEQ 两次注射(LPS 注射前 2 小时和 LPS 注射后一天)时,所有小鼠都被挽救。LPS 注射后 1 小时和 LPS 注射后一天注射 DHMEQ 也导致所有小鼠获救。与仅接受 LPS 的小鼠相比,同时接受 LPS 和 DHMEQ 的小鼠的血清 TNF-α 水平受到抑制。这些结果表明,DHMEQ 可用于预防和治疗内毒素休克。