Huang D, Fang F, Xu F
Department of Pediatric Intensive Care Unit, Guizhou Provincial People's Hospital, GuiYang, China.
Eur Rev Med Pharmacol Sci. 2016 Apr;20(7):1399-410.
It has been reported that inflammation of lung could be induced by proinflammatory factor under hyperoxia, which may be attributed by increasing generation of reactive oxygen species (ROS).
In the present study, with human epithelial lung cancer cell line A549 treated with hyperoxia as in vitro model, we found that hyperoxia stimulation induced TLR2/4 activity in A549 cells. ROS inhibitor NAC was used to investigate the role of ROS in hyperoxia-induced inflammatory cytokines secretion.
Results of mRNA to protein level showed that elevated TLR2/4 activity and hyperoxia-induced inflammatory cytokines secretion could be significantly attenuated by NAC. EMSA results showed the activation of nuclear factor-κB (NF-κB) increased after 2-h hyperoxia stimulation, and the ROS inhibitor blocked TLR2/4 and NF-κB activity.
Data suggested that the TLR2/4-NF-κB pathway is involved in hyperoxia-induced inflammatory cytokines secretion in A549 human type II alveolar epithelial cells.
据报道，高氧环境下促炎因子可诱导肺部炎症，这可能归因于活性氧（ROS）生成增加。
在本研究中，以体外培养的人肺上皮癌细胞系A549为模型，用高氧处理，我们发现高氧刺激可诱导A549细胞中TLR2/4的活性。使用ROS抑制剂NAC来研究ROS在高氧诱导的炎性细胞因子分泌中的作用。
从mRNA水平到蛋白质水平的结果表明，NAC可显著减弱升高的TLR2/4活性和高氧诱导的炎性细胞因子分泌。电泳迁移率变动分析（EMSA）结果显示，高氧刺激2小时后核因子κB（NF-κB）的活性增加，而ROS抑制剂可阻断TLR2/4和NF-κB的活性。
数据表明，TLR2/4-NF-κB信号通路参与了高氧诱导的A549人II型肺泡上皮细胞炎性细胞因子的分泌。
