Ergothioneine inhibits oxidative stress- and TNF-α-induced NF-κB activation and interleukin-8 release in alveolar epithelial cells
Ergothioneine inhibits oxidative stress- and TNF-α-induced NF-κB activation and interleukin-8 release in alveolar epithelial cells
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DOI：
10.1016/s0006-291x(03)00224-9
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发表时间：
2003-03-21
影响因子：
3.1
通讯作者：
Aruoma, OI
中科院分区：
文献类型：
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作者：
Rahman, I;Gilmour, PS;Aruoma, OI
氧化剂和炎症介质如肿瘤坏死因子- α (tnf - α)可激活转录因子如nf - κ b。白细胞介素-8 （IL-8）是一种普遍存在的炎症趋化因子，可介导肺部多种炎症事件。麦角硫因是一种天然存在的硫醇化合物，具有抗氧化特性。本研究的目的是确定麦角硫因是否能抑制人肺泡上皮细胞中过氧化氢(H2O2)-和tnf - α介导的NF-kappaB活化和IL-8释放（A549）。用H2O2 （100 μ m）和tnf - α (10 ng/ml)处理A549细胞可显著增加NF-kappaB的活化。麦角硫因抑制H2O2-和tnf - α介导的nf - κ b活化。H2O2和tnf - α均显著增加IL-8的释放，与未处理的对照细胞相比，麦角硫因预处理A549细胞抑制了IL-8的释放。麦角硫因转染A549细胞后，也能消除IL-8-氯霉素乙酰转移酶（CAT）报告系统中IL-8的转录激活。这提示麦角硫因抗炎作用的分子机制。(C) 2003年Elsevier Science（美国）出版。
Oxidants and inflammatory mediators such as tumour necrosis factor-alpha (TNF-alpha) activate transcription factors such as NF-kappaB. Interleukin-8 (IL-8) is a ubiquitous inflammatory chemokine that mediates a multitude of inflammatory events in the lung. Ergothioneine is a naturally occurring thiol compound, which possesses antioxidant property. The aim of this study was to determine whether ergothioneine can inhibit the hydrogen peroxide (H2O2)- and TNF-alpha-mediated activation of NF-kappaB and the release of IL-8 in human alveolar epithelial cells (A549). Treatment of A549 cells with H2O2 (100 muM) and TNF-alpha (10 ng/ml) significantly increased NF-kappaB activation using a reporter assay. Ergothioneine inhibited both H2O2- and TNF-alpha-mediated activation of NF-kappaB. Both H2O2 and TNF-alpha significantly increased IL-8 release, which was inhibited by pre-treatment of A549 cells with ergothioneine compared to the control untreated cells. Ergothioneine also abolished the transcriptional activation of IL-8 in an IL-8-chloramphenicol acetyltransferase (CAT) reporter system, transfected into A549 cells. This indicates a molecular mechanism for the anti-inflammatory effects of ergothioneine. (C) 2003 Published by Elsevier Science (USA).