心复康口服液对心梗后心衰大鼠心肌组织ANT1 mRNA及蛋白表达的影响

Impacts of Xinfukang Oral Liquid on Myocardial ANT1 mRNA and Protein Expressions in Heart Failure Rats after Cardiac Infarction

目的观察心复康口服液对心肌梗死心衰大鼠心肌组织ANT1 mRNA及ANT1蛋白表达的影响。方法采用结扎SD大鼠左冠状动脉前降支复制心肌梗死后心衰大鼠模型,随机分为模型组、卡托普利组、心复康组,各组于术后24 h灌胃给药至8周;观察各组大鼠梗死周围心肌组织ANT1 mRNA及ANT1蛋白表达水平。结果与模型组比较,卡托普利组、心复康组心肌ANT1 mR-NA、蛋白表达均上调,在第8周末,差异有统计学意义(P<0.01)。与卡托普利组比较,心复康组心肌ANT1 mRNA表达水平在第8周末上调,差异有统计学意义(P<0.05);心复康组心肌ANT1蛋白表达水平在第8周末与卡托普利组比较无显著性差异(P>0.05)。结论心复康口服液可上调心肌梗死后心衰大鼠心肌细胞ANT1 mRNA的表达,促进ANT1蛋白含量增加,达到改善抗充血性心力衰竭(CHF)心肌细胞能量穿梭紊乱,重塑心肌梗死后心衰大鼠心肌能量代谢作用。

Objective To observe the impacts of xinfukang oral liquid on myocardial ANT1 mRNA and ANT1 protein expressions in heart failure rats after myocardial infarction. Methods The rat models of heart failure after myocardial infarction were created by ligating their left anterior descending coronary arteries of SD rats. They were randomized into a model group, a Captopril group and a xinfukang group（ XFK group）. After operation,the medication by gastric infusion was done for 24h till the 8th week in each group. The expressions of ANT1 mRNA and ANT1 protein in infarcted peripheral myocardial tissue of rats were observed in each group. Results Compared with the model group,ANTI mRNA and ANT1 protein expressions were up - regulated in the Captopril group and XFK group. At the end of the 8th week, the difference presented the statistical significance（P 〈 0.01 ）. Compared with the Captopril group, the expression of myocardial ANT1 mRNA was up - regulated at the end of the 8th week in XFK group, indicating the statistically significant difference（P 〈 0.05）. The difference in myocardial ANT1 protein expression at the end of the 8th week in XFK group was not significant as compared with the Captopril group （P 〉 0.05）. Conclusion Xinfukang oral liquid up - regulates myocardial ANT1 mRNA expression and promotes the increase of ANT1 protein ex- pression in heart failure rats after myocardial infarction so as to relieve congestive heart failure and the disorder of myocardial cell energy shuttling and remold myocardial energy metabolism in heart failure rats after myocardial infarction.