摘要
目的研究辅酶Q10联合阿托伐他汀对心衰大鼠氧化作用、心肌重构的影响及其机制。方法左冠状动脉前降支被结扎并饲养6 w的24只大鼠随机分为假手术组、模型组、阿托伐他汀组、辅酶Q10+阿托伐他汀组,每组6只,灌胃给药5 w后测定血清超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量、全心及左室肥厚指数(HW/BW,LVHW/BW)、非梗死区心肌解偶联蛋白2(UCP2)的水平。结果联合应用辅酶Q10及阿托伐他汀能明显升高SOD活性,降低血清MDA的含量及心肌肥厚指数、下调UCP2的水平(P<0.05～0.001)。结论辅酶Q10联合阿托伐他汀可能通过抗氧化作用,下调心肌梗死后心衰大鼠心肌细胞内UCP2的水平,降低心肌肥厚指数,改善心肌重构。
Objective To investigate the mechanism and effects of atorvastatin and coenzyme Q10 on the oxidation and myocardial remodeling in heart failure rats after myocardial infarction（MI）. Methods Thd rat model of heart failure was established by left anterior de- scending coronary artery deligation. After 6 w, 24 surviving rats were divided into sham, model, atorvastatin and atorvastatin ＋ coenzyme groups at random, 6 rats in each, and were treated with medicines by intragastric administration respectively. At 5 w, the activity of serum superexide dismntase （SOD） and the content of serum malondialdehyde（MDA） were measured. The heart weight （HW）and left ventricular heart weight （LVHW）were weighed. HW/BW and LVHW/BW were calculated. Furthermore, the level of uncoupling proteins 2 （UCP2） was detected. Results Atorvastatin association with coenzyme Q10 increased the activity of serum superoxidc dismntase, whereas decreased significantly the content of MDA in serum and myocardial hypertrophy index, downregulated the expression of UCP2. Conclusions Atorvas- tatin association with coenzyme Q10 has improve ventricular remodeling by downregulating the expression of UCP2 on heart failure after AMI in rats, which might be related to scavenging the oxygen free radicals formed.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2013年第7期1571-1573,共3页
Chinese Journal of Gerontology
基金
国家自然科学基金资助项目(No.30770883)
