全烟气致小鼠肺损伤模型的建立
Development of Model for Whole Smoke-induced Lung Injury in Mice
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摘要: 参照国内外采用卷烟烟气致小鼠肺癌等实验模型的程序和方法,应用国产昆明系小鼠建立了全烟气导致肺损伤的模型。将60只小鼠随机分为对照组和吸烟组,吸烟组在染毒箱中全烟气暴露2 h/d,10支烟/次,每支烟燃吸12 min,吸烟机抽吸频率为1次/min,每周6次,连续暴露4个月后解剖,并进行了病理学、免疫组化和蛋白质组学分析。结果表明:①与对照组相比,吸烟组小鼠肺内可见明显炎症细胞浸润,纤毛倒伏、缺失,杯状细胞不同程度增生,肺泡腔大小不一,部分肺泡间隔变薄或断裂,且有明显沉积物存在。②PCNA及p53蛋白表达阳性率分别为80.0%和66.7%,显著高于对照组。③吸烟组小鼠肺部部分水溶性总蛋白表达明显下调,分子量为18.6~23.6 kD的部分蛋白条带含量明显降低。Abstract: Abstract:A model for whole smoke-induced lung injury in Kunming mice was developed by referring to the procedures and methods of experimental models for tobacco smoke-induced lung cancer in mice at home and abroad. Sixty mice were randomly divided into two groups:the control group and the exposed group. The mice of exposed group were exposed to whole smoke within a vessel at the conditions that 10 cigarettes were smoked for 2 hours by smoking machine each day at the frequency of 1 puff/minute and 6 days per week. After 4 months of exposure, the exposed mice were dissected for pathological, immunohistochemical and proteomics analysis. The results showed that:1) Comparing with the control group, the lungs of exposed mice possessed distinct inflammatory cell infiltration, cilia lodging and deficiency, goblet cell hyperplasia of different degrees, alveolar cavities of different sizes, some alveolar septal became thinner or broken, and evident presence of sediment. 2) The positive rates of PCNA and p53 protein expression in exposed mice were 80.0% and 66.7%, respectively, which were significantly higher than those in the control group. 3) The expression of some water-soluble proteins lowered evidently in the lungs of exposed mice, the content of some protein bands with the molecular weight of 18.6-23.6 kD reduced obviously.
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