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机构地区:[1]山西医科大学第二医院,山西省太原市030001 [2]山西医学科学院 [3]山西大医院,山西省太原市030001
出 处:《中国动脉硬化杂志》2012年第10期903-907,共5页Chinese Journal of Arteriosclerosis
基 金:山西省回国留学人员科研资助项目(2010-59)
摘 要:目的探讨阿托伐他汀对高胆固醇血症兔心肌能量代谢的干预作用。方法 24只健康雄性新西兰兔随机分成正常对照组、高胆固醇组和阿托伐他汀组(予高胆固醇饮食并给与阿托伐他汀处理)。喂养6周后,经兔耳缘静脉取空腹血标本测血清总胆固醇的浓度;取心肌组织,电镜观察心肌及线粒体超微结构改变;用高效液相色谱法测心肌线粒体ATP和辅酶Q10含量;用紫外分光光度法测线粒体呼吸链复合物Ⅱ、Ⅳ的活性。结果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,与正常对照组比较,线粒体呼吸链复合物Ⅱ、Ⅳ活性下降,线粒体ATP、辅酶Q10含量减少(P<0.01);阿托伐他汀组与高胆固醇组比较,呼吸链复合物Ⅱ、Ⅳ活性升高(P<0.01),线粒体ATP、辅酶Q10含量差异无统计学意义(P>0.05)。结论阿托伐他汀可减轻高胆固醇血症导致的心肌及线粒体结构损伤,升高线粒体内膜呼吸链复合物Ⅱ、Ⅳ活性,进而改善线粒体氧化磷酸化能力。Aim To observe the intervention of atorvastatin on myocardial energy metabolism in rabbits with hy- perchotesterolemia. Methods Twenty-four male New Zealand white rabbits were randomly divided into three groups: control group, cholesterol group, atorvastatin treated group fed with cholesterol. After feeding for 6 weeks,the empty stom- ach blood preparation through ear marginal vein were collected, the levels of serum total cholesterol were determined;the myocardium was taken to observe its uhrastructures by electron microscopy; High-performance liquid chromatography (HPLC) was used to measure myocardial mitochondria ATP and CoQ10 ;Uhraviolet spectrophotomtry was used to measure the activities of SDH and CCO. Results In cholesterol group there were myocardial fibers derangement, part of the fracture, dissolution, mitochondria swelling, crest disturbance, fuzzy, and Comparing with control group, the activities of SDH and CCO were significantly decreased, the content of myocardial mitochondria ATP and CoQ10 was significantly decreased(P 〈 0. 01 ). Compared with cholesterol group, the activities of SDH and CCO in atorvastatin treated group were increased ( P 〈 0. 01 ), and comparing the content of myocardial mitochondria ATP and CoQ10, there was no significant difference be- tween the two groups (P 〉 0.05). Conclusions Atorvastatin may reduce structure damage of myocardial mitochondri- al cause by hypercholesterolemia,increase the activities of SDH and CCO, thereby improve the oxidative phosphorylation ca- pacity of mitochondrial.
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