大黄素对氧化应激所致动脉粥样硬化模型大鼠的干预研究

Interventional Effect of Emodin on Oxidative Stress-induced Atherosclerosis Model Rats

目的:探讨大黄素对氧化应激所致动脉粥样硬化模型大鼠血脂、血管病理形态等的影响。方法:选择SPF级雄性SD大鼠48只,随机分为6组,每组8只,共饲养12周。正常对照组予普通饲料喂养,其余5组前8周予高脂饲料喂养,建立动脉粥样硬化模型,后4周改为普通饲料喂养,并进行药物干预。大黄素大、中、小剂量组分别给予大黄素80mg/kg、40mg/kg、20mg/kg灌胃。阿托伐他汀组给予阿托伐他汀0.3mg/kg灌胃。高脂模型组和正常对照组给予等量(2 m L)生理盐水灌胃。第12周末处死动物,检测血脂、血清中T-AOC、SOD、MDA的含量;切片观察主动脉壁粥样硬化改变情况。结果:大黄素大、中、小剂量组、阿托伐他汀组血清TC、TG、和LDL均低于高脂模型组(P<0.05),HDL均高于高脂模型组(P<0.05)。黄素大、中、小剂量组、阿托伐他汀组、高脂模型组T-AOC、SOD的含量均高于正常对照组(P<0.05);高脂模型组MDA的含量明显高于其余5组(P<0.05)。动脉组织切片显示,正常对照组动脉壁形态正常,高脂饲料组切片呈动脉粥样硬化,大黄素大剂量组与阿伐他汀组动脉壁形态接近正常。结论:大黄素对氧化应激所致大鼠动脉粥样硬化具有防治作用,其机制可能与抗脂质过氧化有关。

Objective： To explore the effect of emodin on the oxidative stress-induced rat atherosclerosis model in the aspects of blood lipids, the morphology of Hood vessels and so on. Methods： The 48 SPF-leveled male SD rats were randomly divided into six groups （with 8 in each group） and fed for 12 weeks. In the normal control grnup, the rats were given ordinary feed. For the other five groups, in the first 8 weeks, the rats were fed with high-fat diet so as to build an atheroselerosis model. However, during the following 4 weeks, the high-tat diet wouht be replaced by the combination of normal diet and pharmacologic intervention. Emodin wouhl t）e divided into three different dose groups, with 80 mg/kg, 40 mg/kg and 20 mg/kg respectively, each group was given a garage daily. For the atorvastatin group, 0.3 mg/kg atorvastatin was given tbr garage once a day. In terms of the high-fat diet group and normal control group, the rats were peffused with the same volume of saline （2mL） once daily. Then, the animals were killed at the end of 12 week to measure the blood lipid, detect the content of T-ADC, SOD, MDA in blood serum, and observe the change of aortic atheroselerosis through tissue section. Results： （1） The TC, TG and LDL in blood serum have decreased significantly, while the HDL has increased in the emodin group and atnrvastatin grnup （P〈0.05）. （2）The content of T-AOC, SOD is higher in the emodin and atorvastatin group than in the normal control group （P〈0.05）. The eontent of MDA is much higher in high-fat diet group than in other five groups （P〈0.05）. （3） For artery tissue section, the artell wall in normal control group is in a nonnal morphology. In the high-fat diet group, an atherosclerosis has shown on the slice. The artery wall in emodin and atorvastatin group is nearly in a normal morphology. Conclusions： Emodin has a sound and comprehensive intervention effect on atherosclerosis, and the mechanism may be related to the inhibition of lipid peroxidation.