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吸烟致大鼠肺组织RAGE和S100A6蛋白高表达

Up-regulation of RAGE and S100A6 in rats exposed to cigarette smoke

中文摘要英文摘要

长期吸烟不仅导致大鼠肺组织发生明显的病理改变,而且可诱导肺支气管上皮细胞中RAGE和S100A6蛋白的高表达,提示在吸烟致肺癌的过程中,RAGE和S100A6蛋白可能起着重要的介导作用.

igarette 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.

吴昭昭、武彦文、刘海云、童建、聂继华、张素萍

基础医学生物科学研究方法、生物科学研究技术

吸烟可替宁RAGES100A6

cigarette smokecotinineRAGES100A6

吴昭昭,武彦文,刘海云,童建,聂继华,张素萍.吸烟致大鼠肺组织RAGE和S100A6蛋白高表达[EB/OL].(2009-01-08)[2025-05-11].http://www.paper.edu.cn/releasepaper/content/200901-315.点此复制

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