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目的:探讨糖基化磷脂酰肌醇特异性磷脂酶(GPI-PLD)对实验性动脉粥样硬化大鼠血脂水平及血管功能、形态的影响。方法:雄性大鼠随机分为三组,静脉输入生理盐水对照组、高表达GPI-PLD(+)细胞组和GPI-PLD(-)细胞组。高脂喂养与维生素D注射(60万IU/kg)建立大鼠动脉粥样硬化模型。实验第6周末,检测血脂水平(总胆固醇,甘油三酯,低密度脂蛋白、高密度脂蛋白)和血清GPI-PLD活性,观察主动脉病理形态学,检测主动脉对乙酰胆碱诱导的内皮依赖性舒张反应。结果:与生理盐水对照组、GPI-PLD(-)细胞组比较,输入高表达GPI-PLD(+)细胞组大鼠的血GPI-PLD活性增加,总胆固醇、甘油三酯、低密度脂蛋白量减少,而高密度脂蛋白增多(P<0.01);动脉内皮细胞较完整,血管增厚程度明显减轻,泡沫细胞数量明显减少;结论:GPI-PLD可抑制高脂喂养大鼠动脉粥样硬化形成。
Objective: To investigate the effect of glycosyl phosphatidylinositol-specific phospholipase (GPI-PLD) on blood lipid level, vascular function and morphology in experimental atherosclerotic rats. Methods: Male rats were randomly divided into three groups: normal saline control group, high GPI-PLD (+) cell group and GPI-PLD (-) cell group. A rat model of atherosclerosis was established by high fat diet and vitamin D injection (600 000 IU / kg). Blood glucose levels (total cholesterol, triglyceride, low density lipoprotein, high density lipoprotein) and serum GPI-PLD activity were measured at the end of the 6th week of the experiment. Pathological morphology of the aorta was observed and aortic acetylcholine-induced endothelium-dependent Relaxation reaction. Results: Compared with the normal saline group and the GPI-PLD (-) cell group, the GPI-PLD activity in the GPI-PLD (+) group was increased, while the total cholesterol, triglyceride, low density lipoprotein (P <0.01); arterial endothelial cells were more intact and vascular thickening was significantly reduced and the number of foam cells was significantly decreased; Conclusion: GPI-PLD can inhibit atherosclerosis in high fat diet rats form.