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作 者:齐亚飞[1] 徐小明[1] 张科东[1] 李征途[1] 张晨婷[1] 叶婧美[1] 姜华[1] 郑则广[1] 卢文菊[1]
机构地区:[1]广州呼吸疾病研究所呼吸疾病国家重点实验室广州医学院第一附属医院,510120
出 处:《国际呼吸杂志》2012年第15期1154-1157,共4页International Journal of Respiration
基 金:国家教育部长江创新团队项目(20098050700041);广东省自然科学基金团队项目(1035101200300000)
摘 要:目的观察熏烟对小鼠肺组织中Mucl表达的影响,并初步探讨其表达水平的改变与烟雾刺激的关系。方法C57雄性小鼠随机分为熏烟组(8只)和对照组(8只),熏烟处理或正常饲养相同时间后处死小鼠,对支气管肺泡灌洗液(BALF)进行细胞计数、染色和分类,同时测定BALF中肿瘤坏死因子α(TNF-α)水平;通过酶联免疫吸附测定法及蛋白质免疫印迹法对BALF及肺组织中Mucl蛋白水平进行检测。同时对香烟烟雾提取物刺激肺上皮来源的A549细胞后MUCl的表达水平进行了验证。结果与对照组比较,熏烟组小鼠肺组织中出现明显炎症细胞浸润,BALF中的细胞总数、中性粒细胞数、巨噬细胞数均增高。同时,熏烟组小鼠的肺组织及BALF中的Mucl表达水平以及BALF中TNF—α的水平均高于对照组(P〈0.05或P〈0.01)。此外,香烟烟雾提取物刺激A549细胞后,可诱导黏蛋白MUCl表达上升。结论熏烟可以导致小鼠肺组织炎症反应并伴随Mucl的表达水平升高和TNF-α分泌的增加,MUCl表达水平的增加可能与香烟烟雾直接作用于肺上皮细胞有关。Objective To observe the impacts of cigarette smoking on lung Mucl expression and investigate the relationships between Mucl changes and cigarette smoking stimulations in lung. Methods Male C57 mice were randomly divided into cigarette smoking group ( n = 8) and normal control group ( n = 8). After the cigarette smoke exposures or not, the mice were sacrificed and the total and differential cell numbers in bronchoalveolar lavage fluid (BALF) were counted. The level of tumor necrosis factor-~ (TNF-a) in BALF was measured. The Mucl level in BALF and lung was determined with ELISA and Western blot respectively. The lung Mucl changes responded to cigarette smoke exposure were confirmed by detecting the MUC1 levels in cultured human lung epithelial A549 cells treated with cigarette smoke extract. Results The higher Mucl level in lung and BALF was found in cigarette smoke exposed mice (P 〈0.05), accompanied with increases on total cell numbers, neutrophils and macrophages numbers and the level of TNF-a in bronchoalveolar lavage fluid ( P 〈0.05 or P〈0.01). Furthermore, the MUC1 level was upregulated in the cigarette smoke extract treated A549 cells. Conclusions Cigarette smoking induces lung inflammation with upregulations on MUC1 and TNF-α levels. The Muc1 increase might originate from the stimulation of cigarette smoke to the lung epithelial cells.
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