论文部分内容阅读
目的研究阿托伐他汀及辅酶Q10通过抗氧化作用改善心衰大鼠的作用机制。方法结扎大鼠左冠状动脉前降支并饲养6周的24只存活大鼠随机分为假手术组(Shamgroup,n=6)、模型组(Model group,n=6)、阿托伐他汀组(atorvastatin group,n=6)、阿托伐他汀+辅酶Q10组(atorvastatin+coenzyme Q10 group,n=6),连续灌胃给药5周后测定大鼠血流动力学参数,全心及左室肥厚指数(HW/BW,LVHW/BW),血清SOD活性及MDA含量,RT-PCR法测定非梗死区心肌组织UCP2 mRNA表达水平。结果联合应用阿托伐他汀及辅酶Q10更能明显升高左心室内压最大上升、最大下降速率(±dp/dtmax)及SOD活性,降低左心室收缩压(LVSP)、左心室舒张末压(LVEDP)、心肌肥厚指数、血清MDA的含量及下调UCP2 mRNA表达水平(P<0.05-0.001),但对心率(HR)、收缩压(SBP)、舒张压(DBP)无明显影响(P>0.05)。结论阿托伐他汀联合辅酶Q10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 mRNA的表达水平改善心衰心室重构过程中能量代谢。
Objective To study the mechanism of atorvastatin and coenzyme Q10 in improving heart failure in rats by antioxidation. Methods Twenty-four surviving rats were anesthetized with sham operation (Shamgroup, n = 6), model group (n = 6), atorvastatin group Atorvastatin group (n = 6), atorvastatin + coenzyme Q10 group (n = 6), the hemodynamics parameters of rats were measured after 5 weeks of continuous intragastric administration, Hypertrophic index (HW / BW, LVHW / BW), serum SOD activity and MDA content were measured. The expression of UCP2 mRNA in non-infarcted myocardium was detected by RT-PCR. Results The combination of atorvastatin and coenzyme Q10 significantly increased the maximum ± dp / dtmax and ± dp / dtmax and the decrease of left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (P <0.05-0.001), but had no significant effect on heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) (P> 0.05), LVEDP, Hypertrophic index, serum MDA content and UCP2 mRNA expression ). Conclusions Atorvastatin combined with coenzyme Q10 may reduce the expression of UCP2 mRNA in cardiomyocytes in heart failure rats after myocardial infarction and improve the energy metabolism in the process of ventricular remodeling.