Department of Hygiene Toxicology, School of Radiation Medicine and Public Health, Soochow University, The Key Laboratory of Radiation Medicine and Protection of Jiangsu Province, Suzhou City 215123, China.
Environ Toxicol Pharmacol. 2009 Sep;28(2):259-64. doi: 10.1016/j.etap.2009.04.013. Epub 2009 May 4.
Cigarette smoke has been widely investigated in terms of epidemiology and pathological endpoints in relation to human lung diseases and animal study. In this study we exposed Wistar rats to cigarette smoke at concentrations of 20% and 60% to explore potential molecular mechanisms at the protein level. Exposures were conducted twice a day, 5 days a week for 43 weeks. As a major metabolite of nicotine in cigarette, cotinine level in rat urine was determined by HPLC-MS. A dose-dependent analysis indicated that cotinine may be used as an exposure marker of cigarette smoke. Expression of receptor for advanced glycation endproducts (RAGE), an immunoglobulin super family that triggers the intracellular signal cascade reaction leading to inflammation and its ligand S100A6 (calgranulin) in bronchial epithelial cells and lung tissues of rats, were found to be positive correlated with cotinine levels, indicating that RAGE and S100A6 may be attributable to inflammation and oxidative damage caused by cigarette smoke.
香烟烟雾在流行病学和病理学终点方面已被广泛研究，涉及人类肺部疾病和动物研究。在这项研究中，我们将 Wistar 大鼠暴露于 20%和 60%的香烟烟雾中，以探索蛋白质水平的潜在分子机制。暴露每天进行两次，每周 5 天，共进行 43 周。作为香烟中尼古丁的主要代谢物，尿中的可替宁水平通过 HPLC-MS 来确定。剂量依赖性分析表明，可替宁可用作香烟烟雾的暴露标志物。在大鼠支气管上皮细胞和肺组织中，发现晚期糖基化终产物受体 (RAGE)的表达与可替宁水平呈正相关，RAGE 是免疫球蛋白超家族的一员，可引发导致炎症的细胞内信号级联反应，其配体 S100A6（钙粒蛋白）也呈阳性相关，表明 RAGE 和 S100A6 可能归因于香烟烟雾引起的炎症和氧化损伤。
