Zhu Hong, Jia Zhenquan, Li Y Robert
Campbell University Jerry M. Wallace School of Osteopathic Medicine, Buies Creek, NC 27506, USA.
Department of Biology, University of North Carolina, Greensboro, NC 27412, USA.
React Oxyg Species (Apex). 2016;2(6):417-420. doi: 10.20455/ros.2016.875.
The nuclear factor E2-related factor 2 (Nrf2) is known as the chief regulator of cellular antioxidant defenses as well as a suppressor of inflammation. Macrophages act as major players in inflammatory responses. Because oxidative stress and inflammation are two intertwined processes, the anti-inflammatory activity of Nrf2 signaling is believed to result from its upregulation of cellular antioxidant defenses via the antioxidant response element-driven transcription. In a recent article published in Nature Communications (May 23, 2016; doi: 10.1038/ncomms11624), Kobayashi et al. reported that Nrf2 suppresses transcriptional upregulation of pro-inflammatory cytokines independent of its role in regulating cellular antioxidants and redox status. This study by Kobayashi et al. provides novel insights into the molecular basis of Nrf2 acting as a suppressor of inflammation.
核因子E2相关因子2（Nrf2）是细胞抗氧化防御的主要调节因子，也是炎症的抑制因子。巨噬细胞是炎症反应的主要参与者。由于氧化应激和炎症是两个相互交织的过程，Nrf2信号通路的抗炎活性被认为是通过抗氧化反应元件驱动的转录上调细胞抗氧化防御而产生的。在2016年5月23日发表于《自然通讯》（doi: 10.1038/ncomms11624）的一篇文章中，小林等人报道，Nrf2抑制促炎细胞因子的转录上调，这与其在调节细胞抗氧化剂和氧化还原状态中的作用无关。小林等人的这项研究为Nrf2作为炎症抑制因子的分子基础提供了新的见解。
