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Up-regulation of RAGE and S100A6 in rats exposed to cigarette smoke
Zhang Su-ping,Wu Yan-wen,Wu Zhao-zhao,Hai-Yun Liu,Ji-Hua Nie,Tong Jian * #
Soochow University
*Correspondence author
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Funding: 国家自然科学基金,放射性氡及子体健康危害的标志基因筛选（No.30671784,20050285009）
Opened online: 8 January 2009
Accepted by: none
Citation: Zhang Su-ping,Wu Yan-wen,Wu Zhao-zhao.Up-regulation of RAGE and S100A6 in rats exposed to cigarette smoke[OL]. [ 8 January 2009] http://en.paper.edu.cn/en_releasepaper/content/27495
 
 
Cigarette smoke has been widely investigated in terms of epidemiological and pathological observation in relation to human lung diseases. In this study, we established an animal model exposed to cigarette smoke and looked for the potential molecular mechanisms at the protein level. Wistar rats were exposed to cigarette smoke at concentrations of 20% and 60% as the low and high concentration group. The exposure was conducted twice a day、5 days a week for 43 weeks. As a major metabolite of nicotine in cigarette, cotinine in rat urine was determined by LC-MS. A time-and dose-dependent analysis indicated that the cotinine level may be used as a biomarker of smoke exposure. Expression of receptor for advanced glycation endproducts(RAGE), an immunoglobulin superfamily that triggers the intracellular signal cascade reaction leading to inflammation and its ligand S100A6(calgranulin) in bronchial epithelial cells and lung tissues of rats exposed to cigarette smoke, were found to be correlated with the cotinine level, indicating that RAGE and S100A6 may attribute to the inflammation and oxidative damage caused by cigarette smoke.
Keywords:cigarette smoke; cotinine; RAGE; S100A6
 
 
 

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