首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Indole-3-carbinol inhibits LPS-induced inflammatory response by blocking TRIF-dependent signaling pathway in macrophages
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Indole-3-carbinol inhibits LPS-induced inflammatory response by blocking TRIF-dependent signaling pathway in macrophages

机译:吲哚-3-甲醇通过阻断巨噬细胞中的TRIF依赖性信号通路来抑制LPS诱导的炎症反应

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摘要

Indole-3-carbinol (I3C), a natural hydrolysis product of glucobrassicin, is a member of the Brassica family of vegetables and is known to have various anti-cancer activities. In the present study, we assessed in vitro and in vivo anti-inflammatory effects of I3C and its molecular mechanisms. I3C attenuated the production of pro-inflammatory mediators such as NO, IL-6, and IL-1β in LPS-induced Raw264.7 cells and THP-1 cells through attenuation of the TRIF-dependent signaling pathway. Furthermore, I3C suppressed the infiltration of immune cells into the lung and pro-inflammatory cytokine production such as IL-6, TNF-α in broncho-alveolar lavage fluid (BALF) in the LPS-induced acute lung injury mouse model. I3C also suppressed IL-1β secretion in nigericin treated in vivo model. I3C has potent anti-inflammatory effects through regulating TRIF-dependent signaling pathways, suggesting that I3C may provide a valuable therapeutic strategy in treating various inflammatory diseases.
机译:吲哚-3-甲醇(I3C)是葡萄糖br素的天然水解产物,是芸苔属蔬菜家族的成员,并具有多种抗癌活性。在本研究中,我们评估了I3C的体外和体内抗炎作用及其分子机制。 I3C通过减弱TRIF依赖性信号传导途径来减弱LPS诱导的Raw264.7细胞和THP-1细胞中促炎性介质(如NO,IL-6和IL-1β)的产生。此外,在LPS诱导的急性肺损伤小鼠模型中,I3C抑制了免疫细胞向肺的浸润和支气管肺泡灌洗液(BALF)中促炎性细胞因子的产生,例如IL-6,TNF-α。 I3C还抑制了尼日利亚霉素处理的体内模型中的IL-1β分泌。 I3C通过调节TRIF依赖性信号传导途径具有有效的抗炎作用,表明I3C可能为治疗各种炎性疾病提供有价值的治疗策略。

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