Abstract：
PM2.5, as one of the most harmful pollutant in the atmospheric environment and population health, has received much attention. We monitored PM2.5 levels at five sampling sites in the Lanzhou City and collected PM2.5 particles from two representative sites for cytotoxicity experiment. The cytotoxicity of PM2.5 samples on A549 cells and migration ability of the cells were respectively detected by Cell Counting kit-8 (CCK-8) assay and scratch assay. We detected the levels of cellular inflammatory factors and oxidative damage-related biochemical indexes. RT-qPCR was used to detect the mRNA levels of NF-κB and epithelial-mesenchymal transition (EMT)-related genes. We found that the Lanlian Hotel station had the highest PM2.5 annual average concentration. The annual average concentration change curve of PM2.5 showed a roughly \"U\"-shaped distribution during the whole sampling period. The cytotoxicity experiment showed the viability of A549 cells decreased and the scratch healing rate increased in the 200 and 400 μg/mL PM2.5-treated groups. We also found 400 μg/mL PM2.5 induced changes in the mRNA levels of NF-κB and EMT-related genes, the mRNA levels of IKK-α, NIK, and NF-κB in the 400 μg/mL PM2.5 group were higher than those in the control group. The mRNA levels of E-cadherin decreased and α-SMA increased in the 400 μg/mL PM2.5 groups, and the mRNA levels of Fibronectin increased in the 400 μg/mL PM2.5 groups. Moreover, we found hydroxyl radical scavenging ability and T-AOC levels were lower, and LPO levels were higher in the 200 and 400 μg/mL PM2.5 groups, and the SOD activity of cells in the 400 µg/mL PM2.5 group decreased. And compared with the control group, the levels of TNF-α were higher in the 200 and 400 μg/mL PM2.5 groups and the levels of IL-1 were higher in the 400 μg/mL PM2.5 group. The results indicated that the cytotoxicity of atmospheric PM2.5 was related to oxidative damage, inflammatory response, NF-κB activity and EMT.
摘要：
PM2.5作为对大气环境和人群健康危害最大的污染物之一,受到了很多关注。我们监测了兰州市五个采样点的PM2.5水平，并从两个有代表性的采样点收集了PM2.5颗粒进行细胞毒性实验。通过细胞计数试剂盒-8(CCK-8)和划痕试验分别检测PM2.5样品对A549细胞的细胞毒性和细胞的迁移能力。检测细胞炎症因子水平及氧化损伤相关生化指标。RT-qPCR检测NF-κB和上皮间质转化（EMT）相关基因的mRNA水平。我们发现，兰联酒店车站的PM2.5年平均浓度最高。在整个采样期间，PM2.5的年平均浓度变化曲线大致呈“U”形分布。细胞毒性实验表明，在200和400μg/mLPM2.5处理组中，A549细胞的活力降低，划痕愈合率增加。我们还发现400μg/mLPM2.5诱导NF-κB和EMT相关基因的mRNA水平变化,IKK-α的mRNA水平，NIK,400μg/mLPM2.5组NF-κB水平高于对照组。400μg/mLPM2.5组E-cadherinmRNA水平降低,α-SMAmRNA水平升高,400μg/mLPM2.5组纤维连接蛋白mRNA水平升高。此外，我们发现羟自由基清除能力和T-AOC水平较低，和LPO水平在200和400μg/mLPM2.5组中较高，400µg/mLPM2.5组细胞SOD活性下降。与对照组相比，200和400μg/mLPM2.5组TNF-α水平较高，400μg/mLPM2.5组IL-1水平较高。结果表明,大气PM2.5的细胞毒性与氧化损伤有关,炎症反应，NF-κB活性和EMT。
