大气混合污染物所致大鼠肺IFN-γ与CC16水平变化的研究

发布时间：2018-11-20 17:23

【摘要】：前言大气污染一直是世界各国关注的环境问题,但对于大气混合污染物导致肺损伤机制的研究在国内还很少。随着工业的快速发展和人民生活水平的不断提高,工业、生活、交通和建筑等各类排放源排放了大量的烟尘和粉尘粒子,导致大气中可吸入颗粒物(particular matter,PM)的含量逐年增加,其中烟气或工业废气排出的可吸入颗粒物是大气主要的污染源,尤其是直径小于10μm的悬浮颗粒物(PM_(10)),因其直径较小而不受人的鼻腔阻挡,可直接进入呼吸道并存留在肺的深部,不易排出体外。另外,由于燃煤排放的SO_2、NO_2等有毒有害的污染物质也急剧增多。PM_(10)、SO_2、NO_2等混合污染物会随着呼吸进入人体支气管和肺泡,严重损害人体健康。探讨大气污染物导致肺损伤的机制逐渐成为热点问题之一。目前大多数学者认为,大气污染导致的急性肺损伤与机体炎症反应失衡有关。T辅助细胞1(Th-1)以分泌干扰素-γ(interferon-γ,IFN-γ)等促炎因子为主,Th-2细胞以分泌白介素4(interleukin,IL-4)等抗炎因子为主,Th1/Th2类细胞因子的失衡实际上反映了促炎与抗炎的失衡。IFN-γ是由Th-1细胞分泌的一种高活性多功能的糖蛋白,主要介导与细胞毒和局部炎症有关的免疫应答。在免疫应答中,IFN-γ可促使Th-1细胞向Th-2细胞分化,抑制Th-2细胞因子的产生,因而可以调节急性炎症发展的方向与转归。克拉氏细胞分泌蛋白(Clara cell secretory 16-kD protein,CC16)是Clara细胞最主要的分泌物,在肺和支气管的表达水平最高,支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中浓度也较高。本研究以大气颗粒物PM_(10)、SO_2、NO_2、CO为综合处理因素,模拟大气混合污染物导致肺损伤的动物模型,通过测定BALF中CC16与IFN-γ水平,探讨大气混合污染物所致肺损伤的机制。
[Abstract]:Air pollution is an environmental problem all over the world, but there are few researches on the mechanism of lung injury caused by mixed air pollutants in China. With the rapid development of industry and the continuous improvement of people's living standard, a great deal of smoke and dust particles have been emitted from various emission sources, such as industry, living, transportation and construction, resulting in (particular matter, in the atmosphere. The content of PM) increases year by year, and the respirable particulates from flue gas or industrial waste gas are the main pollution sources of the atmosphere, especially the suspended particulates with diameter less than 10 渭 m (PM_ (10),) is not blocked by human nasal cavity because of its small diameter. Can directly enter the respiratory tract and remain in the deep lung, not easy to expel from the body. In addition, the toxic and harmful pollutants such as SO_2,NO_2 and other pollutants emitted from coal have increased rapidly. PM_ (10), SO_2,NO_2 and other mixed pollutants will enter the human bronchi and alveoli with breathing, which will seriously damage human health. Exploring the mechanism of lung injury caused by atmospheric pollutants has gradually become one of the hot issues. At present, most scholars believe that the acute lung injury caused by air pollution is related to the imbalance of inflammatory reaction. T-helper cell 1 (Th-1) mainly secretes pro-inflammatory factors such as interferon- 纬 (IFN- 纬). Th-2 cells mainly secrete anti-inflammatory factors such as interleukin 4 (interleukin,IL-4). The imbalance of Th1/Th2 cytokines actually reflects the imbalance between proinflammatory and anti-inflammatory. IFN- 纬 is a highly active multifunctional glycoprotein secreted by Th-1 cells, which mainly mediates the immune response related to cytotoxicity and local inflammation. In the immune response, IFN- 纬 can induce the differentiation of Th-1 cells into Th-2 cells and inhibit the production of Th-2 cytokines, thus regulating the development direction and outcome of acute inflammation. Clariot cell secretory protein (Clara cell secretory 16-kD protein,CC16) is the most important secretion of Clara cells, the highest expression level is in lung and bronchi, and the concentration in bronchoalveolar lavage fluid (bronchoalveolar lavage fluid,BALF) is also higher than that in bronchoalveolar lavage fluid (BALF). In this study, PM_ (10) and SO_2,NO_2,CO were used as comprehensive treatment factors to simulate the animal model of lung injury induced by mixed air pollutants. The levels of CC16 and IFN- 纬 in BALF were measured. To investigate the mechanism of lung injury induced by mixed air pollutants.
【学位授予单位】：中国医科大学
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R361

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