Suppr超能文献

促炎 NF-κB 和早期生长反应基因 1 通过食品添加剂角叉菜胶调节人肠上皮细胞的上皮屏障破坏。

Pro-inflammatory NF-κB and early growth response gene 1 regulate epithelial barrier disruption by food additive carrageenan in human intestinal epithelial cells.

机构信息

Laboratory of Systems Mucosal Biomodulation, Department of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea.

出版信息

Toxicol Lett. 2012 Jun 20;211(3):289-95. doi: 10.1016/j.toxlet.2012.04.012. Epub 2012 Apr 26.

Abstract

The widely used food additive carrageenan (CGN) has been shown to induce intestinal inflammation, ulcerative colitis-like symptoms, or neoplasm in the gut epithelia in animal models, which are also clinical features of human inflammatory bowel disease. In this study, the effects of CGN on pro-inflammatory transcription factors NF-κB and early growth response gene 1 product (EGR-1) were evaluated in terms of human intestinal epithelial barrier integrity. Both pro-inflammatory transcription factors were elevated by CGN and only NF-κB activation was shown to be involved in the induction of pro-inflammatory cytokine interleukin-8. Moreover, the integrity of the in vitro epithelial monolayer under the CGN insult was maintained by both activated pro-inflammatory transcription factors NF-κB and EGR-1. Suppression of NF-κB or EGR-1 aggravated barrier disruption by CGN, which was associated with the reduced gene expression of tight junction component zonula occludens 1 and its irregular localization in the epithelial monolayer.

摘要

食品添加剂卡拉胶(CGN)在动物模型中已被证实可诱导肠道炎症、溃疡性结肠炎样症状或肿瘤,这些也是人类炎症性肠病的临床特征。在这项研究中,评估了 CGN 对人肠道上皮屏障完整性的促炎转录因子 NF-κB 和早期生长反应基因 1 产物(EGR-1)的影响。促炎转录因子均被 CGN 上调,且仅 NF-κB 激活被证明参与诱导促炎细胞因子白细胞介素-8 的产生。此外,CGN 刺激下体外上皮单层的完整性可通过激活的促炎转录因子 NF-κB 和 EGR-1 来维持。NF-κB 或 EGR-1 的抑制加重了 CGN 引起的屏障破坏,这与紧密连接成分闭合蛋白 1 的基因表达减少及其在上皮单层中的不规则定位有关。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验