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目的:观察大气环境中细颗粒物对血管内皮功能的影响,探索细颗粒物作用于心血管疾病的途径和机制,同时使用阿托伐他汀进行干预,观察药物对内皮损伤的作用。方法:将细颗粒物使用0.9%氯化钠配制成浓度为4000μg/ml的悬浮液,对人脐静脉血管内皮细胞(Endothelial cells,EC-304)进行染毒,染毒终浓度为400μg/ml,观察细颗粒物对EC-304细胞存活率、细胞内丙二醛(Malondial dehyde,MDA)、细胞裂解液中超氧化物歧化酶(Superoxide dismutase,SOD)及细胞上清液中一氧化氮(Nitrous oxide,NO)等的影响。同时使用阿托伐他汀钙药物进行干预,在染毒细胞中加入0.1μmol/L,1μmol/L和10μmol/L剂量浓度的阿托伐他汀钙,测定药物对上述指标的影响。结果:细颗粒物有机提取物染毒后,EC-304的存活率明显下降、细胞上清液MDA明显升高、细胞内SOD及细胞上清液中NO较对照组明显下降(P<0.01)。染毒后加入阿托伐他汀钙能明显改善细颗粒物对血管内皮细胞的毒性作用,使EC-304上清液MDA较对照组明显下降,而细胞存活率、细胞内SOD及细胞上清液中NO较对照组增加,并有剂量-反应关系(P<0.01)。结论:细颗粒物对EC-304具有明显的损害作用,环境因素如细颗粒物在心血管疾病的发生发展中起着不可忽视的作用,同时使用他汀类药物可以改善血管内皮功能,促进心血管疾病的功能恢复,论证了他汀类药物可改善细颗粒物导致血管内皮损伤的药理作用。
OBJECTIVE: To observe the effects of fine particulate matter (PM) on vascular endothelial function in the atmospheric environment and to explore the ways and mechanisms of fine particulate action on cardiovascular diseases. Atorvastatin intervention was also performed to observe the effect of drugs on endothelial injury. Methods: The fine particles were formulated into a suspension with the concentration of 4000μg / ml by using 0.9% sodium chloride, and the human umbilical vein endothelial cells (EC-304) were exposed to a final concentration of 400μg / ml. To observe the effect of fine particles on the survival rate of EC-304 cells, intracellular malondialdehyde (MDA), superoxide dismutase (SOD) in cell lysate and nitrous oxide NO) and other effects. In the meantime, atorvastatin calcium was used for intervention. At doses of 0.1μmol / L, 1μmol / L and 10μmol / L of atorvastatin calcium were added into the infected cells to determine the effect of the drug on these indexes. Results: The survival rate of EC-304 cells was significantly decreased after exposure to the organic extract of fine particles. The content of MDA in the supernatant of the cells was significantly increased, and the levels of SOD in the cells and NO in the supernatant were significantly decreased (P <0.01). The addition of atorvastatin calcium after exposure could obviously improve the toxicity of fine particles to vascular endothelial cells, and the MDA content in EC-304 supernatant decreased significantly compared with control group. However, the cell viability, intracellular SOD and cell supernatant NO increased compared with the control group, and dose-response relationship (P <0.01). CONCLUSIONS: Fine particulate matter has obvious damage to EC-304. Environmental factors such as fine particulate matter play an important role in the development of cardiovascular diseases. At the same time, statins can improve endothelial function and promote cardiovascular function Restoration, demonstrating the pharmacological effects of statins can improve fine particles lead to vascular endothelial injury.