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目的探讨罗格列酮辛伐他汀对动脉粥样硬化兔内皮功能的影响。方法40只日本大耳白兔随机分为五组,正常对照组、高脂模型组、罗格列酮组、辛伐他汀组、联合用药组,每组8只。A组(正常对照组):普通颗粒饲料喂饲150g,日二次,10周。B组(高脂模型组):高脂饲料(1%胆固醇+8%猪油+普通颗粒饲料)150g,日二次,10周。C组(罗格列酮组):高脂饲料喂饲10周,从喂饲高脂饲料起,给予口服罗格列酮0.5mg/kg/日。D组(辛伐他汀组):高脂饲料喂饲10周,从喂饲高脂饲料起,给予口服辛伐他汀2.0mg/kg/日。E组(联合用药组):高脂饲料喂饲10周,从喂饲高脂饲料起,给予口服罗格列酮0.5mg/kg/日+辛伐他汀2.0mg/kg/日。实验结束后获取血浆和主动脉全长标本进行生化和病理分析。结果高脂模型组、各用药组与正常对照组相比血清血脂、内皮素(ET-1)水平增高,一氧化氮(NO)浓度降低,主动脉内膜不同程度脂质斑块形成,模型组最明显。罗格列酮组、辛伐他汀组、联合用药组三组ET-1浓度明显低于高脂模型组,NO水平高于高脂模型组,P<0.01,联合用药组效果最显著;四组主动脉可见不同程度的脂质斑块形成,其斑块/内膜面积比高脂模型组>罗格列酮组>辛伐他汀组>联合用药组,P<0.01。结论罗格列酮、辛伐他汀通过改善内皮功能、调脂等各自不同途径防治动脉硬化的发生发展,并具有协同作用。
Objective To investigate the effect of rosiglitazone and simvastatin on endothelial function in atherosclerotic rabbits. Methods Forty Japanese white rabbits were randomly divided into five groups: normal control group, high fat model group, rosiglitazone group, simvastatin group and combination group. Group A (normal control group): ordinary pellet feed 150g, day two, 10 weeks. Group B (high fat model group): high fat diet (1% cholesterol + 8% lard + ordinary pellet feed) 150g, twice daily for 10 weeks. Group C (rosiglitazone group): high-fat diet for 10 weeks, fed with high-fat diet, given oral rosiglitazone 0.5mg / kg / day. Group D (simvastatin group): High-fat diet was fed for 10 weeks, and orally administered simvastatin 2.0 mg / kg / day was given from high-fat diet. Group E (combination group): high-fat diet for 10 weeks, fed with high-fat diet, given oral rosiglitazone 0.5mg / kg / day + simvastatin 2.0mg / kg / day. After the experiment, the full-length specimens of plasma and aorta were obtained for biochemical and pathological analysis. Results Compared with the normal control group, the levels of serum lipids, endothelin (ET-1), nitric oxide (NO) and the formation of lipid plaque in the aortic intima were significantly increased in the model group and the control group The most obvious group. The concentrations of ET-1 in rosiglitazone group, simvastatin group and combination group were significantly lower than those in high-fat model group, and the NO level was higher than that in high-fat model group (P <0.01) Aortic plaques showed different degrees of plaque formation. The area of plaque / intima was higher in the model group than in the rosiglitazone group, simvastatin group and combination group (P <0.01). Conclusions Rosiglitazone and simvastatin can prevent and cure the occurrence and development of atherosclerosis by improving endothelial function and lipid regulation, and have synergistic effects.