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目的:观察天香丹对ApoE(-/-)基因敲除小鼠高脂血症及动脉粥样硬化的影响。方法:将30只8周龄的ApoE(-/-)基因敲除小鼠随机分为模型组、天香丹组和阿托法汀组,每组各10只,另以相同遗传背景的同龄正常C57BL/6J小鼠为正常对照组(n=10)。天香丹组每只灌服天香丹7.2g.kg-1.d-1,阿托伐他汀组每只灌服阿托伐他汀10 mg.kg-1.d-1,模型组和正常对照组每只灌服0.9%生理盐水0.2ml.10g-1.d-1。连续灌胃12周后眼眶采血测定各组血脂含量,取小鼠主动脉弓部进行形态学观察及图像分析。结果:模型组血清总胆固醇、甘油三酯和低密度脂蛋白水平明显高于正常对照组(P<0.05),而天香丹组和阿托伐他汀组以上3项指标与模型组相比明显下降(P<0.05)。图像分析测量结果显示模型组与正常对照组比较其斑块总面积明显增加(P<0.05);天香丹组动脉硬化病变程度较模型组减轻,其斑块总面积明显减小(P<0.05)。结论:天香丹有降低ApoE(-/-)基因敲除小鼠血清总胆固醇、甘油三酯和低密度脂蛋白胆固醇水平及减缓动脉粥样硬化病变的作用。
Objective: To observe the effect of Tianxiangdan on hyperlipidemia and atherosclerosis in ApoE (- / -) knockout mice. Methods: Thirty 30-week-old ApoE (- / -) knockout mice were randomly divided into model group, Tianxiangdan group and Atorvastatin group, with 10 in each group. Normal mice of the same genetic background with normal age C57BL / 6J mice were normal control group (n = 10). Days Xiangdan group were given Tianxiangdan 7.2g.kg-1.d-1, atorvastatin group were given atorvastatin 10 mg.kg-1.d-1, the model group and the normal control group Each fed 0.9% saline 0.2ml.10g-1.d-1. After 12 weeks of continuous gavage, orbital blood sampling was performed to measure the blood lipid levels in each group. Morphological observation and image analysis were performed on the aortic arch of mice. Results: The levels of serum total cholesterol, triglyceride and low density lipoprotein in the model group were significantly higher than those in the normal control group (P <0.05), while those in the Tianxiangdan group and the atorvastatin group were significantly lower than those in the untreated group (P <0.05). The results of image analysis showed that the total area of plaque in model group was significantly increased compared with that in normal control group (P <0.05). The degree of atherosclerosis in model group was lower than that in model group, and the plaque area was significantly decreased (P <0.05) . CONCLUSION: Tianxiangdan can reduce serum total cholesterol, triglyceride and low density lipoprotein cholesterol levels and attenuate atherosclerotic lesions in ApoE (- / -) knockout mice.