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目的:探讨辅酶Q10对动脉粥样硬化模型大鼠血脂及主动脉斑块内白细胞介素6(IL-6)、脂蛋白磷脂酶A2(lipoprotein-phospholipase A 2,LP-PLA2)、可溶性细胞间粘附分子-1(s ICAM-1)表达的影响。方法 :将35只Wistar大鼠随机分为正常空白对照组、动脉粥样硬化模型组、辅酶Q10组、阿托伐他汀组、辅酶Q10+阿托伐他汀组。空白对照组大鼠予常规饲料喂养,其余4组大鼠行动脉粥样硬化建模成功后,辅酶Q10组、阿托伐他汀组、辅酶Q10+阿托伐他汀组大鼠分别给药8周,取动脉血及完整主动脉,检测血脂水平,采用连续法检测血清对氧磷酶1及LP-PLA2活性,酶联免疫吸附试验检测血清氧化型高密度脂蛋白(HDL)及丙二醛含量。取主动脉根部,用免疫组织化学法及蛋白印迹法检测IL-6、LP-PLA2及s ICAM-1表达量。结果:与空白对照组相比,动脉粥样硬化模型组的血清三酰甘油、胆固醇、低密度脂蛋白(LDL)、载脂蛋白B及氧化型HDL、丙二醛水平均明显上升,而HDL水平、血清对氧磷酶1活性下降,LP-PLA2活性增高,斑块内IL-6、LP-PLA2及s ICAM-1表达增加,差异均有统计学意义(P<0.05)。经辅酶Q10处理后,辅酶Q10组大鼠血清三酰甘油、胆固醇及载脂蛋白B较动脉粥样硬化模型组变化差异无统计学意义,但HDL上升,LDL下降,血清对氧磷酶1活性增加和LP-PLA2活性下降,血清氧化型HDL及丙二醛下降,主动脉斑块内IL-6、LP-PLA2、s ICAM-1表达显著下降(P<0.05),另辅酶Q10可增强阳性对照药阿托伐他汀的效果(P<0.05)。结论:辅酶Q10可增加动脉粥样硬化大鼠的血清HDL含量,改善其HDL功能,降低其体内的氧化应激水平和影响主动脉炎症因子的表达,从而可能发挥抑制动脉粥样硬化形成及减少斑块破裂的作用。
Objective: To investigate the effects of coenzyme Q10 on serum lipids and interleukin 6 (IL-6), lipoprotein-phospholipase A2 (LP-PLA2), soluble intercellular Effects of adhesion molecule-1 (s ICAM-1) expression. Methods: 35 Wistar rats were randomly divided into normal control group, atherosclerosis model group, coenzyme Q10 group, atorvastatin group, coenzyme Q10 + atorvastatin group. The rats in blank control group were fed with conventional diet, and the rats in the other four groups were given a model of atherosclerosis and were successfully treated with coenzyme Q10, atorvastatin and coenzyme Q10 + atorvastatin for 8 weeks, Serum paraffinase and intact aorta were taken for determination of serum lipid levels. Serum paraoxonase 1 and LP-PLA2 activities were measured by continuous method. Serum levels of oxidized high density lipoprotein (HDL) and malondialdehyde (MDA) were measured by enzyme linked immunosorbent assay. The aortic root was taken and the expression of IL-6, LP-PLA2 and s ICAM-1 was detected by immunohistochemistry and Western blot. Results: Serum triglyceride, cholesterol, low density lipoprotein (LDL), apolipoprotein B, oxidized HDL and malondialdehyde in atherosclerotic model group were significantly higher than those in the blank control group, while HDL The levels of serum paraoxonase 1, the activity of LP-PLA2 and the expression of IL-6, LP-PLA2 and s ICAM-1 in plaque increased significantly (P <0.05). Coenzyme Q10 treatment, coenzyme Q10 group serum triglyceride, cholesterol and apolipoprotein B than atherosclerosis model group was no significant difference, but HDL increased LDL decreased serum paraoxonase 1 activity LP-PLA2 and sICAM-1 expression in aortic plaque decreased significantly (P <0.05), coenzyme Q10 could enhance the expression of IL-6, LP-PLA2 and s ICAM- Control drug atorvastatin effect (P <0.05). CONCLUSION: Coenzyme Q10 can increase the level of serum HDL in atherosclerosis rats, improve its HDL function, reduce its oxidative stress level and affect the expression of aortic inflammatory factors, and thus may inhibit the formation and decrease of atherosclerosis The role of plaque rupture.