摘要
目的 探索PM2. 5颗粒物引起心血管疾病的机制。方法 ECV30 4细胞暴露于不同浓度的PM2. 5颗粒物混悬液 (5 0、2 0 0、4 0 0 μg/ ml) ,染毒 2 4小时后运用MTT法测细胞存活率、测定细胞内SOD和GSH含量、并进行流式细胞仪分析凋亡来综合分析。结果 随着染毒浓度上升 ,ECV30 4细胞存活率逐渐下降 ,死亡率逐渐上升 ;染毒浓度为 5 0、2 0 0、4 0 0 μg ml,细胞内GSH含量 (mg gprot)分别为 2 0 . 6 4 3± 2 .16 7、16. 774± 2 911(P <0. 0 5 )、15. 6 5 8± 3. 4 71(P <0. 0 1) ,SOD含量 (U mgprot)为 5. 878± 0. 4 0 1、5 14 0± 0 . 4 4 8(P <0 .0 1)、4 . 817± 0 . 4 5 1(P <0 . 0 1)。结论 PM2. 5可通过氧化损伤途径使血管内皮细胞死亡 ,导致心血管疾病的发生。
Objective\ To study the mechanism of cardiovascular d isease affected b y PM 2.5. Methods ECV304 cells were exposed to PM 2.5 of different concentration(5 0,200 and 400μg/ml), after 24h, the viability of cells by MTT, SOD and GSH cont ents in cells and apoptosis of cells determined by flow cytometer were measured. Results Viability of ECV304 cells declined and mortality of EC V304 cells increa sed gradually with increase of concentration, GSH contents in cells (mg/g prot ) were 20.643±2.167,16.774±2.911(P<0.05),15.658±3.471(P<0.01), and SOD content s in cells (U/mg prot ) were 5.878±0.401,5.140±0.448(P<0.01),4.817 ±0.451(P<0 .01) when the concentration of PM 2.5 was 50,200 and 400μg/ml. C onclusion PM 2.5 can cause vascular endothelial cells to die by way of oxidative injury, then ind uce cardiovascular disease.
出处
《卫生研究》
CAS
CSCD
北大核心
2005年第2期169-171,共3页
Journal of Hygiene Research
基金
国家自然科学基金资助项目 (No .30 2 71 1 0 6)
