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首页> 外文期刊>Cellular immunology >Sodium azide suppresses LPS-induced expression MCP-1 through regulating I kappa B zeta and STAT1 activities in macrophages
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Sodium azide suppresses LPS-induced expression MCP-1 through regulating I kappa B zeta and STAT1 activities in macrophages

机译：叠氮化钠通过调节巨噬细胞的κBZeta和Stat1活性来抑制LPS诱导的表达MCP-1

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摘要

Sodium azide (NaN3) is a chemical compound with multiple toxic effects on vascular and neuronal systems, causing hypotension and neurotoxicity, respectively. In order to test its effects on the immune system, human and mouse macrophage-like cell lines were treated with nontoxic doses of NaN3 and the changes in LPS-induced inflammatory activation was measured. Interestingly, the LPS-induced expression of monocyte chemoattractant protein (MCP)-1 was suppressed by NaN3 without affecting the expression of IL-8 and TNF-alpha. Further analysis of cellular signaling mediators involved in the expression of these cytokines revealed that NaN3 suppressed the LPS-induced activation of signal transducers and activator of transcription (STAT) 1 and inhibitor of kappa B (I kappa B)zeta , which are involved in the LPS-induced expression of MCP-1, while the LPS-induced activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) was not affected. The LPS-induced expression of MCP-2 and CXCL10, which are also regulated by STAT1, was suppressed by NaN3. Similarly, the LPS-induced expression of IL-6, which is regulated by I kappa B zeta, was suppressed by NaN3. These results demonstrate that NaN3 selectively suppresses the LPS-induced expression of pro-inflammatory mediators through the suppression of STAT1 and I kappa B zeta activation. These new findings about the activity of NaN3 may contribute to the development of specific regulators of macrophage activity during acute and chronic inflammation.
机译：叠氮化钠（NAN3）是一种对血管和神经元系统具有多种毒性作用的化合物，分别引起低血压和神经毒性。为了测试其对免疫系统的影响，用无毒剂量的NAN3处理人和小鼠巨噬细胞样细胞系，并测量LPS诱导的炎症活化的变化。有趣的是，通过NAN3抑制了单核细胞化学蛋白（MCP）-1的LPS诱导的表达，而不影响IL-8和TNF-α的表达。进一步分析涉及这些细胞因子表达的细胞信号传导介质揭示了NaN3抑制了LPS诱导的信号传感器和转录激活剂的激活（统计学）1和Kappa B（I Kappa B）Zeta的抑制剂，其参与其中LPS诱导MCP-1的表达，而LPS诱导的活化B细胞核因子Kappa-Light链增强剂的活化（NF-Kappa B）未受影响。 NAN3抑制了由STAT1调节的MCP-2和CXCL10的LPS诱导的表达。类似地，通过NaN 3抑制了由I Kappa B Zeta调节的IL-6的LPS诱导的表达。这些结果表明，NaN3通过抑制Stat1和I Kappa B Zeta活化选择性地抑制促炎介质的LPS诱导的表达。关于NAN3的活性的这些新发现可能有助于在急性和慢性炎症期间发育巨噬细胞活性的特定调节因子。

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  • 来源
    《Cellular immunology》 |2017年第2017期|共7页
  • 作者

    Park Cho-Yi; Heo Jae-Nyoung; Suk Kyoungho; Lee Won-Ha;

  • 作者单位

    Kyungpook Natl Univ Plus KNU Creat BioRes Grp BK21 Sch Life Sci Daegu 41566 South Korea;

    Kyungpook Natl Univ Plus KNU Creat BioRes Grp BK21 Sch Life Sci Daegu 41566 South Korea;

    Kyungpook Natl Univ Sch Med Plus KNU Biomed Convergence Program BK21 Dept Pharmacol Brain Sci &

    Kyungpook Natl Univ Plus KNU Creat BioRes Grp BK21 Sch Life Sci Daegu 41566 South Korea;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    LPS; MCP-1; Signaling; Macrophage; STAT1; I kappa B zeta;

    机译：LPS;MCP-1;信令;巨噬细胞;STAT1;I Kappa B Zeta;

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