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[目的]通过体外细胞实验观察大气细颗粒物不同成分对血管内皮细胞的氧化损伤作用,进而了解其对心血管系统的毒作用机制。[方法]提取细颗粒物水溶成分、非水溶成分和有机提取物对人脐静脉血管内皮细胞(endothelialcells,EC-304)进行染毒,各成分染毒剂量均设为100、200、400μg/mL3个剂量组;另设药物干预组:细颗粒物3种成分染毒剂量均为400μg/mL,同时加入10μmol/L浓度的阿托伐他汀钙药物。测定染毒后细胞存活率和细胞内丙二醛(malondialdehyde,MDA)含量,并对染毒后细胞内超氧化物歧化酶(superoxide dismutase,SOD)和活性氧(reactive oxygen species,ROS)的变化进行定性和定量观察。[结果]经大气细颗粒物3种成分染毒后,EC-304细胞存活率明显下降,细胞内MDA随颗粒物染毒剂量升高而升高。细胞内SOD在染毒1h时即出现下降,并随染毒剂量升高而降低,且染毒剂量相同时,水溶成分的毒作用高于有机提取物,亦高于非水溶成分。随着染毒剂量的增加,细胞内ROS明显增加(P<0.01),且有机提取物和水溶成分产生ROS的能力明显高于非水溶成分(P<0.01)。加入阿托伐他汀钙后,细胞内MDA和ROS较未加药物组明显降低,SOD则明显增加。[结论]大气细颗粒物不同成分能导致血管内皮细胞出现氧化损伤,呈剂量-反应关系,氧化损伤可能是大气细颗粒物心血管毒性的作用机制之一。
[Objective] The purpose of this study was to observe the effect of different components of atmospheric fine particles on the oxidative damage of vascular endothelial cells by in vitro cell experiments and to understand its toxic mechanism on cardiovascular system. [Method] The water soluble, water-insoluble and organic extracts of fine particulate matter were extracted to infect human umbilical vein endothelial cells (EC-304). The doses of each component were set at 100, 200 and 400 μg / mL Dose group; another drug intervention group: fine particles of three components were dose of 400μg / mL, while adding 10μmol / L concentration of atorvastatin calcium drugs. The cell viability and intracellular malondialdehyde (MDA) contents were determined after exposure to the above chemicals and the changes of superoxide dismutase (SOD) and reactive oxygen species (ROS) Qualitative and quantitative observation. [Results] The survival rate of EC-304 cells was significantly decreased after exposure to the three components of fine particles of the atmosphere, and the intracellular MDA increased with the increase of the dose of particulate matter. Intracellular SOD decreased at 1 h and decreased with the increase of exposure dose. The toxicity of water soluble components was higher than that of organic extracts at the same dosage, and higher than that of non-water soluble components. With the increase of exposure dose, intracellular ROS increased significantly (P <0.01), and the ability of organic extracts and water soluble components to produce ROS was significantly higher than that of non-water soluble components (P <0.01). Adding atorvastatin calcium, intracellular MDA and ROS decreased significantly compared with no drug group, SOD increased significantly. [Conclusion] Different components of airborne fine particles can cause oxidative damage of vascular endothelial cells in a dose-response relationship. Oxidative damage may be one of the mechanisms of cardiovascular toxicity of fine particulate matter in the atmosphere.