摘要
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 explore the protective effects and mechanisms of pravastatin on impairment of vascular endothelium cells induced by lysophosphatidyl choline （LPC）. Methods： The models of both isolated thoracic aortic rings of rats and cultured human endothelial cells （HUVECs） were used. The endothelial-dependent and non-dependent relaxation and the content of malondialdehyde （MDA） in vascular tissues, and vitality of endothelial cells and the biochemical indexes were measured. Results： LPC decreased markdly endothelial-dependent relaxation response （EDR） and increased significantly content of MDA in vascular tissue. The incubation of rings with pravastatin concentration-dependently improved significantly endothelial-dependent relaxation response （EDR） injuried by LPC, but did not affect the non-endothelial dependent. Simultaneously pravastatin obviously prevented the increase of the MDA in vascular tissue and the ROS in cultured HUVECs, and inhibited the increase of vitality of endothelial cells and reduction of both eNOS activity and NO content induced by LPC in cultured HUVECs. Conclusions： LPC could directly inhibit endothelial-dependent relaxation induced by Ach. Pravastatin may concentration-dependently improve the impairment of endothelial function damaged by LPC. The action mechanismes of pravastatin may be related to antioxidant and antiinflammatory defenses.
出处
《现代生物医学进展》
CAS
2009年第22期4350-4353,4311,共5页
Progress in Modern Biomedicine
关键词
普伐他汀
溶血磷脂酰胆碱
内皮依赖性舒张反应
内皮细胞
活性氧簇
Lovastatin
Lysophosphatidyl Choline
Endothelium-Dependent Relaxation
Endothelial Cells
Reactive Oxygen Species
