论文部分内容阅读
目的:探讨不同剂量的普伐他汀对溶血磷脂酰胆碱(LPC)所致血管内皮功能的影响。方法:用离体血管环和培养的人脐静脉内皮细胞(HUVECs)为实验模型,以血管内皮依赖性舒张反应(EDR)、内皮细胞活力以及生化参数为指标,用LPC作为损伤因子,用普伐他汀作为保护药,观察LPC对内皮的损伤作用及普伐他汀的保护作用。结果:LPC与血管环共孵或内皮细胞显著性地抑制了血管EDR反应,增加了血管MDA含量,并导致培养的内皮细胞的活力、内皮型一氧化氮合酶(eNOS)活性及一氧化氮(NO)含量显著性降低;普伐他汀与血管环或内皮细胞共孵,浓度依赖性地减轻了LPC对血管EDR的抑制作用(P<0.05),保护了内皮细胞的活力(P<0.05),恢复了细胞eNOS活性及NO含量(P<0.05),抑制了内皮细胞活性氧(ROS)的生成(P<0.05)。结论:LPC能直接损伤的血管内皮细胞,普伐他汀对LPC所致的血管内皮细胞损伤有显著性保护作用,其机制可能与LPC触发脂质过氧化反应,从而抑制血管内皮血管内皮细胞NO的合成有关,普伐他汀通过抗氧化而保护血管内皮细胞的功能。
Objective: To investigate the effects of different doses of pravastatin on endothelial function induced by lysophosphatidylcholine (LPC). Methods: In vitro vascular rings and cultured human umbilical vein endothelial cells (HUVECs) were used as experimental models. Endothelial-dependent vasodilation (EDR), endothelial cell viability and biochemical parameters were used as indexes. LPC was used as an injury factor, As a protective drug, we observed the injury of endothelial cells by LPC and the protective effect of pravastatin. RESULTS: LPCs incubated with vascular rings or endothelial cells significantly inhibited the vascular EDR response, increased vascular MDA content and resulted in endothelial cell activity, endothelial nitric oxide synthase (eNOS) activity and nitric oxide (P <0.05), and the activity of endothelial cells was significantly reduced (P <0.05). Conclusions: Pravastatin, which was incubated with vascular rings or endothelial cells, attenuated the inhibitory effect of LPC on blood vessel EDR in a concentration- , Restored the activity of eNOS and the content of NO (P <0.05), inhibited the production of reactive oxygen species (ROS) in endothelial cells (P <0.05). Conclusion: LPC can directly damage vascular endothelial cells and pravastatin have a significant protective effect on LPC-induced vascular endothelial cell injury. The mechanism may be associated with LPC triggering lipid peroxidation, thus inhibiting the expression of NO in vascular endothelial cells Synthesis, pravastatin through the antioxidant and protect the function of vascular endothelial cells.