| With the rapid development of industrialization and urbanization, the usage of coal and oil fuel also increased strongly, then the urban air pollution problem become more prominent and constitute a badly threat to human health. The air pollutants such as particulate matter of atmosphere, SO2, NO2, CO and so on were closely related to the human health, among them, the PM2.5 was a kind of composite pollutant with complex components formed of large amount of different chemicals from man-made pollution and natural source, the toxicity of PM2.5 had prominent relationship with its chemical constituents,and heavy metal and charcoal were the main constituents of it. Air pollutants were closely related to human health, especially to the respiratory and circulatory system. Human clara cells were mainly distribute in epithelium of bronchiole terminates and respiratory bronchiole, CC16 was one of the 20 kinds of protein secreted by alveolar epithelium, and its main function was to prevent infringe of pollutants to alveolar epithelium, so the testing of CC16 was very valuable in evaluate injury of air-blood barrier or its integrity, it was very important in basic and clinical medical research.Objective:To explore the toxic effect mechanism of atmospheric pollutants (PM2.5, SO2, NO2, CO) to injury of lung tissue, this experiment mainly finded out the CC16 level in mouse blood serum and pulmonary tissue under the effect of mixed air pollutants via dustexposure and contamination method, in order to provide bases in preventing injury of air pollution to human body.Methods:78 Wistar rats were randomly divided into 6 guoups due to their weight,3 experiment groups (Id,7d,30d),3 control groups (1d,7d,30d),13 rats in each group.Rats were injected into non-open stance trachea with dust exposure method after anaesthetized with ether,1 ml saline suspl with 10 mg PM2.5 for experiment groups and 1 ml saline for control groups. Experiment groups were gived dynamic inhalation of air mixed with SO2, NO2, CO of 15,12, 400 mg/m3 for 4h per day, and lasted for Id,7d,30d in different experiment groups, and control groups were gived inhalation of normal air. ELISA method was utilized to determine the CC16 level in serum and BALF, real time RT-PCR method was used to detect the expression level of GC16 in lung tissue, immunohistochemistry method was used to determine the CC16 level in lung tissue.Results:1. CC16 expression in lung tissue of rats contaminated for Id and 30d were obviously higher than their control groups, AOD value had statistic significance (P<0.01). CC16 expression in lung tissue of rats contaminated for 7d was obviously lower than it's control group, AOD value had statistic significance(P<0.01). Comparison within experiment groups, CC16 expression in lung tissue of rats contaminated for 7d was obviously lower than that for Id, there was statistic significance (P< 0.01).CC16 expression in lung tissue of rats contaminated for 30d was obviously higher than that for Id, there was statistic significance (P < 0.01).CC16 expression in lung tissue of rats contaminated for 30d was obviously higher than that for 7d, there was statistic significance (P< 0.01).2. CC16mRNA expression in lung tissue of rats contaminated for Id had no obviously change compared with it's control group, there was no statistic significance (P> 0.05). CC16mRNA expression in lung tissue of rats contaminated for 7d was higher than it's control group, there had statistic significance (P< 0.05).CC16mRNA expression in lung tissue of rats contaminated for 30d had no obviously change compared with it's control group, there was no statistic significance (P> 0.05). Comparison within experiment groups, CC16mRNA expression in lung tissue of rats contaminated for 1d and 30d were both lower than that for 7d, there had statistic significance (P< 0.05).3. CC16 content in serum of rats contaminated for Id was a little lower than it's control group, but there was no statistic significance (P> 0.05).CC16 in serum of rats contaminated for 7d was a little lower than it's control group, but there was no statistic significance (P> 0.05). CC16 in serum of rats contaminated for 30d was obviously higher than it's control group and that had statistic significance (P< 0.05). Compared within experiment groups, CC16 in serum of rats contaminated for 7d was a little higher than that for 1d, but there was no statistic significance (P> 0.05), CC16 in serum of rats contaminated for 7d and 1d were obviously lower than that for 30d, that had statistic significance (P< 0.05). 4. CC16 content in BALF of rats contaminated for Id,7d and 30d had no obviously change compared with their control groups, there was no statistic significance (P> 0.05).CC16 in BALF of rats contaminated for Id,7d and 30d had no obviously change compared each other, there was no statistic significance (P> 0.05).Conclusions:1. In the early inflammatory reactions due to atmospheric pollutants (Id), the CC16 in lung tissue of rats were obviously higher than that in control groups but the CC16 in serum and BALF nearly had no change, then we can know that early inflammatory reactions may lead to increase of CC16 in lung tissue.2. Endothelial Contaminated for 7d, the CC16 in rats'pulmonary tissue were obviously lower than that in control groups, that due to severe injury of lung tissue cells and endothelial cells of capillaries. And the CC16mRNA expressions were obviously higher than that in control groups expressed that in the 7d injury, the CC16mRNA expression compensatory increased,so the CC16mRNA level can be a kind of sensitive biologic index of early lung injury.3. Contaminated for 30d, the CC16 in serum increased obviously, that means the self-repair of alveolus and the compensatory increase of CC16 compose which at last resulted in the CC 16 increase in serum.4. The CC16 in lung tissue decrease was an important index of early lung injury and the increase of CC16 express that the pulmonary tissue had entered into a repairing process. Unchanged CC 16 in BALF means that the CC16 in BALF can not be an index in determinant of lung injury. |
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