...
首页> 外文期刊>Toxicology in vitro: an international journal published in association with BIBRA >Fluoride as a factor initiating and potentiating inflammation in THP1 differentiated monocytes/macrophages
【24h】

Fluoride as a factor initiating and potentiating inflammation in THP1 differentiated monocytes/macrophages

机译:氟化物是引发和增强THP1分化单核细胞/巨噬细胞炎症的因素

获取原文
获取原文并翻译 | 示例
           

摘要

It is well known that exposure to fluorides lead to an increased ROS production and enhances the inflammatory reactions. Therefore we decided to examine whether cyclooxygenases (particular COX-2) activity and expression may be changed by fluoride in THP1 macrophages and in this way may change the prostanoids biosynthesis. In the present work we demonstrate that fluoride increased concentration of PGE(2) and TXA(2) in THP1 macrophages. Following exposure to 1-10 mu M NaF, COX-2 protein and COX-2 transcript increased markedly. COX-2 protein up-regulation probably is mediated by ROS, produced during fluoride-induced inflammatory reactions. Additional fluoride activates the transcription factor, nuclear factor (NF)-kappaB, which is involved in the up-regulation of COX-2 gene expression. This study indicated that even in small concentrations fluoride changes the amounts and activity of COX-1 and COX-2 enzymes taking part in the initiating and development of inflammatory process. (C) 2015 Elsevier Ltd. All rights reserved.
机译:众所周知,暴露于氟化物会导致ROS产生增加,并增强炎症反应。因此,我们决定检查THP1巨噬细胞中的环氧合酶(特别是COX-2)的活性和表达是否可能被氟化物改变,并以此方式改变前列腺素的生物合成。在目前的工作中,我们证明了氟化物会增加THP1巨噬细胞中PGE(2)和TXA(2)的浓度。暴露于1-10μMNaF后,COX-2蛋白和COX-2转录物显着增加。 COX-2蛋白的上调可能是由氟介导的炎症反应过程中产生的ROS介导的。额外的氟化物激活转录因子,核因子(NF)-κB,其参与COX-2基因表达的上调。这项研究表明,即使在低浓度下,氟化物也会改变参与炎症过程的发生和发展的COX-1和COX-2酶的数量和活性。 (C)2015 Elsevier Ltd.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号