论文部分内容阅读
目的:探讨阿托伐他汀对C57BL/6J小鼠动脉粥样硬化的影响机制。方法:将24只雄性C57BL/6J小鼠随机分为对照组、模型组和药物干预组。12周后酶法和免疫比浊法检测血清甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)和apoA-I;HE染色观察主动脉病理形态学改变;高效液相色谱法检测动脉壁胆固醇含量;PepTag@Assay法检测蛋白激酶C活性变化;Westernblot检测动脉壁CD36蛋白表达。结果:相较于模型组,阿托伐他汀可以显著下调血清总胆固醇和LDL胆固醇水平,上调血清apoA-I水平,抑制胆固醇在血管壁的蓄积,降低内膜/中膜厚度比,下调动脉壁蛋白激酶C活性和CD36蛋白表达,有效地抑制了动脉粥样硬化的发展。结论:阿托伐他汀可能是通过抑制胆固醇合成、下调蛋白激酶C活性和CD36蛋白表达而发挥降脂、消斑、改善动脉壁功能的作用。
Objective: To investigate the mechanism of atorvastatin on atherosclerosis in C57BL / 6J mice. Methods: 24 male C57BL / 6J mice were randomly divided into control group, model group and drug intervention group. Twelve weeks later, serum triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and apoA-I The morphological changes of the aorta were observed by HE staining. The contents of cholesterol in arterial wall were detected by HPLC. The changes of protein kinase C activity were detected by PepTag @ Assay. The expression of CD36 was detected by Western blot. Results: Compared with model group, atorvastatin significantly down-regulated serum total cholesterol and LDL cholesterol levels, raised serum apoA-I level, inhibited the accumulation of cholesterol in the vascular wall, decreased intima / media thickness ratio and down-regulated arterial wall Protein kinase C activity and CD36 protein expression, effectively inhibit the development of atherosclerosis. Conclusion: Atorvastatin may play an important role in lowering arterial wall function by inhibiting cholesterol synthesis, down-regulating protein kinase C activity and CD36 protein expression.