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目的筛选敏感的生物标志物,探讨大气混合污染物对肺泡II型上皮细胞(AT-II)的损伤及其机制,为控制大气污染的危害提供理论依据。方法使用便携式PM2.5采样器和47mm玻璃纤维滤膜采集大气粉尘样品,制成生理盐水混悬液,实验大鼠气管注入混悬液及动态吸入SO2、NO2、CO混合气,制备大气混合污染物吸入动物模型,测定染毒不同时间血清及支气管肺泡灌洗液(BALF)中肺表面活性蛋白(SP-A)水平,肺组织中SP-A的mRNA及蛋白表达。结果染毒7 d组大鼠肺组织中SP-A mRNA表达为1.816±1.299,明显高于染毒1、30 d组(0.930±0.587;0.902±0.378)及对照组;染毒30 d组大鼠肺组织中SP-A表达吸光度值为0.385±0.068,明显低于染毒7 d组(0.438±0.069)及对照组;染毒30 d组大鼠BALF中SP-A水平为47.09±5.78,明显低于染毒1、7 d组(54.72±6.15;58.82±9.76)及对照组;染毒30 d组大鼠血清中SP-A水平明显高于染毒1、7 d组及对照组。结论 SP-A是反映AT-II功能受损严重程度的肺特异性指标。
Objective To screen sensitive biomarkers and investigate the damage and mechanism of airborne pollutants to alveolar type II epithelial cells (AT-II), so as to provide a theoretical basis for controlling the harm of air pollution. Methods A portable PM2.5 sampler and a 47mm glass fiber filter were used to collect atmospheric dust samples and made into physiological saline suspension. Trachea was injected into the suspension and the mixture of SO2, NO2 and CO was dynamically inhaled to prepare air pollution The animal model of superoxide dismutase was inhaled. The level of SP-A and the expression of SP-A mRNA and protein in lung tissue were measured at different time points. Results The SP-A mRNA expression in the lung tissue of rats exposed to 7 d was 1.816 ± 1.299, which was significantly higher than that in the control group (0.930 ± 0.587; 0.902 ± 0.378, The SP-A expression level in rat lung tissue was 0.385 ± 0.068, which was significantly lower than that in control group (0.438 ± 0.069) and control group. SP-A level in BALF was 47.09 ± 5.78 The level of SP-A in the serum of the rats in the 30th day of exposure was significantly higher than that in the 1st and 2nd day of exposure (54.72 ± 6.15; 58.82 ± 9.76) and the control group. Conclusions SP-A is a lung-specific marker that reflects the severity of AT-II dysfunction.