燃煤PM2.5不同组分对血管内皮细胞的氧化损伤效应

摘要

To explore the effects of different compositions of fine particles on the cardiovascular system. Coal sample taking Datong coal as a sample, Coal-fired PM2.5 was sampled by fixed source dilution channel in the laboratory. All particles, as well as isolated inorganic and organic compositions, were extracted to contaminate EA.hy926cells for 24h respectively. To evaluate oxidative damages of different compositions of coal-fired PM2.5 exposed to the EA.hy926cells, the assays of superoxide dismutase (SOD), malondialdehyde (MDA), Glutathione peroxidase (GSH-Px) were carried out using assay kits according to the manufacturer’s instructions. The results showed that as the dose increased, SOD activity decreased in EA.hy926exposed to different compositions of coal-fired PM2.5 24h. Each dose group was statistically different (P<0.01) compared with the control group, and there is a dose-response relationship. At the same dose, SOD inhibition of different compositions was: organic compounds> inorganic compositions > all particles, with statistically significance differences among the same dose. Compared to solvent control, as the dose increased, GSH-Px activity decreased in EA.hy926exposed to different compositions of coal-fired PM2.5. At the same dose, GSH-Px inhibition of different compositions was:inorganic compounds>organic compositions>all particles, with no statistically significance differences. As the dose increased, MDA levels in supernatants treated with all particles, inorganic compositions and organic compositions increased, respectively. At the low doses, MDA level of different compositions of coal-fired PM2.5 on EA.hy926was:organic compositions>all particles>inorganic compositions, while at the high doses:all particles>inorganic compositions > organic compositions with statistically significance, and as the dose increased, MDA level caused by all particles and inorganic compositions increased significantly, while changes of organic compositions is leveling off. The results can be seen from the above, different compositions of PM2.5exerted oxidative damage to EA.hy926 ,reduced activities of SOD, GSH-Px, and increased MDA level. But the mechanisms underlying them need futher exploration.%为了解细颗粒物不同组分在心血管系统损伤中的毒性机制,以大同散煤为样品煤,提取燃煤 PM 2.5全颗粒物、无机组分及有机组分,分别对人脐静脉内皮细胞EA.hy926进行染毒,采用超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)及丙二醛(MDA)指标检测PM 2.5不同组分对EA.hy926细胞氧化损伤程度的影响.结果表明,燃煤PM 2.5各组分对EA.hy926细胞染毒24h后,随着染毒剂量的增加,细胞上清液中SOD活力均下降,与对照组相比差异显著,而相同剂量组比较,其抑制SOD活力能力依次为：有机组分>无机组分>全颗粒物,且相同剂量组不同组分间的比较均有统计学差异；GSH-Px活力均下降,具有剂量依赖性,引起GSH-Px活力下降程度基本具有无机组分>有机组分>全颗粒物的趋势,但统计学意义不显著；MDA 含量分别有不同程度的增加,各组分所致的 MDA 含量大小存在低剂量组有机组分>全颗粒物>无机组分,高剂量组全颗粒物>无机组分>有机组分趋势,随着剂量增加,全颗粒物和无机组分引起MDA含量明显增加,而有机组分则变化趋于平缓.可见,燃煤PM不同组分均对血管内皮细胞EA.hy926氧化损伤作用明显,SOD 、GSH-PX等抗氧化酶的活性降低.2.5 inorganic compositions > organic compositions with statistically significance, and as the dose increased, MDA level caused by all particles and inorganic compositions increased significantly, while changes of organic compositions is leveling off. The results can be seen from the above, different compositions of PM2.5exerted oxidative damage to EA.hy926,reduced activities of SOD, GSH-Px, and increased MDA level. But the mechanisms underlying them need futher exploration.