Qu Run-bo, Lu Yu-sa, Gong Fei-yu
Department of Cardiology, Second Hospital, Shanxi Medical University, Taiyuan, China.
Zhonghua Yi Xue Za Zhi. 2012 Jul 10;92(26):1854-7.
To explore the interventional effects of atorvastatin and CoQ(10) on myocardial energy metabolism in rabbits with hypercholesterolemia.
Forty male New Zealand white rabbits were randomly divided into 5 groups: i.e. normal control, high cholesterol, statin, coenzyme Q(10) 1 and coenzyme Q(10) 2. After feeding for 6 weeks, the fasting blood samples were collected through ear marginal vein and the serum level of total cholesterol was determined. Myocardium was sampled for ultrastructures by electron microscopy; high-performance liquid chromatography (HPLC) was used to measure myocardial mitochondria adenosine triphosphate (ATP) and coenzyme CoQ(10). Ultraviolet spectrophotometry was used to measure the activities of mitochondrial complexes II and IV.
In high cholesterol group, myocardial fibers were arrayed disorderly with partial rupture and dissolution. There was mitochondrial swelling with disorderly and fuzzy cristae. As compared with the controls, the activities of mitochondrial respiratory chain complexes II and IV declined (5.39 ± 0.53 vs 12.95 ± 0.99, 1.89 ± 0.26 vs 6.65 ± 0.95, P < 0.01), the contents of mitochondrial ATP and CoQ(10) decreased (0.17 ± 0.05 vs 0.44 ± 0.06, 0.09 ± 0.02 vs 0.25 ± 0.04, P < 0.01); for statin group versus high cholesterol group, the activities of mitochondrial respiratory chain complexes II and IV increased (9.12 ± 1.19 vs 5.39 ± 0.53, 4.61 ± 0.52 vs 1.89 ± 0.26, P < 0.01); the content differences of mitochondrial ATP and CoQ(10) were statistically insignificant. For CoQ(10) 1 group versus statin group, the differences of respiratory chain complexes II and IV were statistically insignificant; the contents of mitochondria ATP and CoQ(10) increased (0.35 ± 0.03 vs 0.16 ± 0.04, 0.17 ± 0.02 vs 0.07 ± 0.02, P < 0.01). For coenzyme Q(10) 2 group versus coenzyme Q(10) 1 group, none of the indices was statistically significant.
High cholesterol can cause myocardial ultrastructural changes and impaired mitochondrial energy metabolism. Atorvastatin reduces the myocardial structural damage and the combination of atorvastatin and CoQ(10) may further improve the myocardial mitochondrial energy metabolism.
探讨阿托伐他汀和辅酶Q10对高胆固醇血症家兔心肌能量代谢的干预作用。
将40只雄性新西兰白兔随机分为5组：正常对照组、高胆固醇组、他汀组、辅酶Q10 1组和辅酶Q10 2组。喂养6周后，经耳缘静脉采集空腹血样，测定血清总胆固醇水平。取心肌组织进行电镜超微结构观察；采用高效液相色谱法（HPLC）测定心肌线粒体三磷酸腺苷（ATP）和辅酶Q10含量。采用紫外分光光度法测定线粒体复合物Ⅱ和Ⅳ的活性。
高胆固醇组心肌纤维排列紊乱，部分断裂溶解。线粒体肿胀，嵴紊乱、模糊。与对照组相比，线粒体呼吸链复合物Ⅱ和Ⅳ的活性下降（5.39±0.53对12.95±0.99，1.89±0.26对6.65±0.95，P<0.01），线粒体ATP和辅酶Q10含量降低（0.17±0.05对0.44±0.06，0.09±0.02对0.25±0.04，P<0.01）；他汀组与高胆固醇组相比，线粒体呼吸链复合物Ⅱ和Ⅳ的活性升高（9.12±1.19对5.39±0.53，4.61±0.52对1.89±0.26，P<0.01）；线粒体ATP和辅酶Q10含量差异无统计学意义。辅酶Q10 1组与他汀组相比，呼吸链复合物Ⅱ和Ⅳ的差异无统计学意义；线粒体ATP和辅酶Q10含量升高（0.35±0.03对0.16±0.04，0.17±0.02对0.07±0.02，P<0.01）。辅酶Q10 2组与辅酶Q10 1组相比，各项指标差异均无统计学意义。
高胆固醇可导致心肌超微结构改变及线粒体能量代谢受损。阿托伐他汀可减轻心肌结构损伤，阿托伐他汀与辅酶Q10联合应用可能进一步改善心肌线粒体能量代谢。
