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目的:应用原子力显微镜(atomic force microscope,AFM)观察动脉粥样硬化(atherosclerosis,As)血管内皮细胞(vascular endothelialcell,VEC)膜超微结构的动态演变情况,以及探讨阿托伐他汀保护血管内皮功能的非降脂作用。方法:取88只新西兰纯种雄性大白兔,随机分为3组,对照组24只喂以普通兔饲料、高脂模型组32只喂以高脂饲料、药物组32只喂以高脂饲料同时给与阿托伐他汀,分别于2、4、6、8周末每组随机处死6-8只。取胸主动脉中段制作标本,应用AFM进行扫描。结果:对照组VEC呈梭形,排列规整,其长轴与血液流动方向一致。高脂模型组随时间不同内皮细胞发生了动态改变,细胞形态变成球形、不规则形、体积变大,排列紊乱。1μm、500nm扫描范围细胞膜超微结构也有明显的改变。药物组VEC的变化在相应的时间段明显好于高脂模型组,基本接近对照组。同时比较了三组500nm水平下膜蛋白的平均粗糙度(meanroughness,Ra),发现在高脂组明显高于正常对照组和药物组,具有统计学差异(P<0.01),阿托伐他汀组细胞膜粗糙度高于正常对照组(P<0.01)。结论:As形成过程中VEC膜超微结构发生了明显的动态变化,而阿托伐他汀可早期预防As引起的内皮细胞损伤,从而阻止As的进一步形成。
OBJECTIVE: To observe the dynamic changes of the ultrastructure of vascular endothelial cells (VECs) in atherosclerosis (As) by atomic force microscope (AFM) and to investigate the protective effect of atorvastatin on vascular endothelial function Non-lipid-lowering effect. Methods: Totally 88 New Zealand white male rabbits were randomly divided into 3 groups. In control group, 24 rabbits were fed with normal rabbits, 32 rabbits in high fat model group were fed with high fat diet, 32 rabbits in high fat diet were fed with high fat diet Given atorvastatin, respectively, at the end of 2, 4, 6, 8, each group were randomly executed 6-8. Take the middle part of the thoracic aorta specimens, the application of AFM scanning. Results: In the control group, the VECs were spindle-shaped and arranged regularly. The long axis of the VECs was in the same direction as the blood flow. In the model group, the endothelial cells changed dynamically with the passage of time. The morphology of the cells changed into spherical shape, irregular shape, larger volume and disordered arrangement. 1μm, 500nm scanning range of cell membrane ultrastructure also have significant changes. VEC changes in the drug group in the corresponding time period was significantly better than the high-fat model group, basically close to the control group. The meanroughness (Ra) of three groups of membrane proteins at 500 nm was also compared, and it was found that there was a statistically significant difference (P <0.01) in the hyperlipidemia group compared with the normal control group and the drug group. The atorvastatin group The cell membrane roughness was higher than that of the normal control group (P <0.01). CONCLUSION: The ultrastructural changes of VEC membrane during As formation are obviously dynamic, while atorvastatin can prevent As-induced endothelial cell injury in the early stage and prevent further formation of As.