Li Min, Guo Lingli, Wang Hao, Wang Tao, Shen Yongchun, Liao Zenglin, Wen Fuqiang, Chen Lei
Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, Sichuan, China.
Department of Respiratory Medicine, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, Sichuan, China.
Respirology. 2015 Aug;20(6):998-9. doi: 10.1111/resp.12557. Epub 2015 May 22.
Receptor for advanced glycation end products (RAGE) was recently shown to contribute to cigarette smoke (CS)-induced airway inflammation in chronic obstructive pulmonary disease (COPD). In this study, RAGE small interfering ribonucleic acid (RNA) transfection attenuated increased messenger RNA levels of common RAGE ligands HMGB1, S100A8, S100A9 and S100A12, but not S100B following exposure to CS extract. Our findings and those from recent studies suggest a positive feedback involving RAGE and its ligands as a new 'driving force' for CS-induced airway inflammation in COPD.
晚期糖基化终末产物受体（RAGE）最近被证明在慢性阻塞性肺疾病（COPD）中促成香烟烟雾（CS）诱导的气道炎症。在本研究中，暴露于CS提取物后，RAGE小干扰核糖核酸（RNA）转染减弱了常见RAGE配体HMGB1、S100A8、S100A9和S100A12的信使核糖核酸水平升高，但未减弱S100B的信使核糖核酸水平升高。我们的研究结果以及最近的研究结果表明，涉及RAGE及其配体的正反馈作为COPD中CS诱导气道炎症的一种新的“驱动力”。
