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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 investigate the effects of emodin on the blood lipid and vascular pathological changes of atherosclerosis model rats induced by oxidative stress. Methods: Forty-eight SPF male Sprague-Dawley rats were randomly divided into 6 groups with 8 rats in each group for 12 weeks. The normal control group was fed with normal feed, and the remaining 5 groups were fed with high-fat diet for the first 8 weeks to establish the model of atherosclerosis. Four weeks later, the rats were fed with normal feed and the drugs were intervened. Emodin large, medium and small dose groups were given emodin 80mg / kg, 40mg / kg, 20mg / kg gavage. Atorvastatin group was given atorvastatin 0.3mg / kg gavage. The model group and the normal control group were given equal volume (2 m L) of normal saline. At the end of the 12th week, the animals were sacrificed, the levels of serum lipids, serum T-AOC, SOD and MDA were measured. The change of aortic wall atherosclerosis was observed by section. Results: The serum levels of TC, TG and LDL in large, medium and small doses of emodin group and atorvastatin group were lower than those in high fat model group (P <0.05), and HDL were higher than those in high fat model group (P <0.05) . The contents of T-AOC and SOD in large, middle and low dose groups, atorvastatin group and high fat model group were significantly higher than those in normal control group (P <0.05); MDA content in high fat model group was significantly higher than the rest 5 groups (P <0.05). Arterial sections showed that the morphology of arterial wall in normal control group was normal, the sections of high-fat diet group was atherosclerosis, and the morphology of arterial wall in high-dose emodin group and atorvastatin group was close to normal. CONCLUSION: Emodin can prevent and cure atherosclerosis in rats induced by oxidative stress, and its mechanism may be related to anti-lipid peroxidation.