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目的研究瑞舒伐他汀对动脉内膜损伤的糖尿病大鼠血脂、动脉粥样硬化和屏氧酶-1(PON1)的作用及其机制。方法 Wistar大鼠48只,随机分为正常对照组、模型组和瑞舒伐他汀组,均n=16。正常对照组给予普通饮食32 wk后生理盐水灌胃2 mo,模型组与瑞舒伐他汀组高脂饮食20 wk后采用链脲佐菌素诱导糖尿病辅助球囊损伤主动脉内膜制模,继续高脂饮食12 wk后分别给予生理盐水和瑞舒伐他汀20 mg.kg-1灌胃2 mo。观察血脂和主动脉内膜形态学改变,并检测PON1的含量、mRNA表达及活性改变。结果与正常对照组相比,模型组大鼠主动脉内膜增生明显,总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)水平明显增高(P<0.01),高密度脂蛋白胆固醇(HDL-C)水平明显降低(P<0.01),PON1表达减少,活性显著下降(P<0.01);与模型组相比,瑞舒伐他汀组TC、TG、LDL-C均显著降低(P<0.05或P<0.01),HDL-C水平呈上升趋势(P>0.05),主动脉内膜增生改善,PON1活性增高、mRNA表达增加(P<0.05或P<0.01)。结论瑞舒伐他汀可降低血脂,通过增加PON1的表达及活性提高HDL-C抗氧化能力,达到延缓动脉粥样硬化的作用。
Objective To investigate the effect and mechanism of rosuvastatin on blood lipid, atherosclerosis and Pox1 in diabetic rats with intimal injury. Methods Forty-eight Wistar rats were randomly divided into normal control group, model group and rosuvastatin group, all with n = 16. Rats in the normal control group were given normal saline for 2 months after oral administration of normal diet for 32 weeks. The rats in model group and rosuvastatin group were treated with streptozotocin-induced diabetes mellitus-aortic intimal injury after 20 weeks of high-fat diet, After 12 weeks of high-fat diet, saline and rosuvastatin 20 mg.kg-1 were given respectively for 2 months. The changes of blood lipid and aorta intima were observed, and the content of PON1, mRNA expression and activity were detected. Results Compared with the normal control group, the aortic intima hyperplasia, the total cholesterol (TC), the triglyceride (TG) and the low density lipoprotein cholesterol (LDL-C) were significantly increased in the model group (P <0.01) , HDL-C (P <0.01) and PON1 expression decreased significantly (P <0.01). Compared with the model group, the levels of TC, TG, LDL- C were significantly lower (P <0.05 or P <0.01), HDL-C level was increased (P> 0.05), aortic intimal hyperplasia was improved, PON1 activity was increased, mRNA expression increased . Conclusion Rosuvastatin can reduce blood lipids and increase the antioxidant capacity of HDL-C by increasing the expression and activity of PON1, which can delay the effects of atherosclerosis.