大气细颗粒物(PM2.5)对心血管内皮细胞NOS的影响

运用体外试验方法,探讨了大气细颗粒物的心血管毒性及其可能的作用机制采集上海城区大气中的PM25,并以0.01、0.05、0.2、1 mg·mL-1剂量染毒大鼠心血管内皮细胞24 h后,观察PM2.5对心血管内皮细胞内总NOS,iNOS及cNOS活力等指标的影响.发现与对照组相比,0.2 mg·mL-1染毒组的心血管内皮细胞总NOS和iNOS活力显著增加,而cNOS活力显著降低,并且随着PM25染毒剂量的增加,存在剂量-反应关系.这一结果表明,PM2.5可通过诱导心血管内皮细胞的iNOS活性,对心血管系统产生氧化应激损伤,氧化应激作用可能是PM2.5心血管系统毒性的作用机制之一.

Study on oxidation stress effects of PM2.5 on cardiovascular endothelium cells

Exposure to PM_2.5 was found to be significantly correlated with the increasing cardiovascular disease mortality in recent epidemiological studies. But there have had little experimental studies to explore the potential mechanism of this adverse effect of PM_2.5 until now. In this study, cardiovascular endothelium cells were treated by PM_2.5 collected from urban area of Shanghai, with doses of 0.01,0.05,0.2 and 1 mg·mL^-1. Parameters (including activities of total NOS, iNOS and cNOS) reflecting the oxidation stress damage were measured. Results showed that the activities of total NOS and iNOS in cardiovascular endothelium cells treated with 0.2 mg mL^-1 PM_2.5 were significantly higher than those in control cells. Dose-response relationship was established in this study. These results meant that PM_2.5 could induce the activity of iNOS in cardiovascular cells and the oxidation stress damage might be one of the mechanisms of PM_2.5 effect on cardiovascular system.