| 廖骏,沈玮芸,孙启银,柳元化.冠心宁治疗急性心肌梗死后心力衰竭大鼠的作用机制研究[J].浙江中西医结合杂志,2023,33(12): |
| 冠心宁治疗急性心肌梗死后心力衰竭大鼠的作用机制研究 |
| Study on the mechanism of Guanxinning in treating heart failure rats after acute myocardial infarction |
| 投稿时间：2023-01-08 修订日期：2023-11-21 |
| DOI： |
| 中文关键词: 急性心肌梗死 心力衰竭 大鼠 冠心宁 炎症反应 心功能 |
| 英文关键词:Acute myocardial infarction heart failure Rats Guanxinning Inflammatory reaction Cardiac function |
| 基金项目:2021年浙江省医学会临床科研(2021ZYC-A136) |
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| 中文摘要: |
| 目的 观察冠心宁治疗急性心肌梗死后心力衰竭大鼠的作用机制。方法 通过结扎左冠状动脉前降支的方法建立大鼠急性心肌梗死后心力衰竭模型,将造模成功的45只大鼠采用随机数字表法分为空白对照组、氯吡格雷组及冠心宁组,每组各15只。灌胃4周后,观察各组大鼠心肌超微结构变化,检测心肌组织中磷脂酰肌醇3-激酶(PI3K)、蛋白激酶B(AKT)表达、心肌组织中氧化应激因子[活性氧(ROS)、细胞总抗氧化能力(T-AOC)]、血清肿瘤坏死因子-α(TNF-α)、转化生长因子-β1(TGF-β1)、心脏彩超指数[左室室间隔收缩期厚度(IVSs)、左室室间隔舒张期厚度(IVSd)、左室短轴缩短率(LVFS)]。结果 相较空白对照组,氯吡格雷组及冠心宁组大鼠的心肌超微结构变化更显著,且冠心宁组对大鼠心肌超微结构的炎性损伤明显减轻。氯吡格雷组、冠心宁组心肌组织中PI3K、AKT表达均高于空白对照组,且冠心宁组高于氯吡格雷组(P＜0.05)。氯吡格雷组、冠心宁组心肌组织中PI3K、AKT表达均低于空白对照组,冠心宁组低于氯吡格雷组(P＜0.05)。氯吡格雷组、冠心宁组心肌组织中ROS低于空白对照组,T-AOC水平高于空白对照组,冠心宁组心肌组织中ROS低于氯吡格雷组,T-AOC水平高于氯吡格雷组(P＜0.05)。氯吡格雷组、冠心宁组血清TNF-α水平低于空白对照组,TGF-β1水平高于空白对照组,冠心宁组血清TNF-α水平低于氯吡格雷组,TGF-β1水平高于氯吡格雷组(P＜0.05)。氯吡格雷组、冠心宁组IVSs低于空白对照组,LVFS高于空白对照组,冠心宁组IVSs低于氯吡格雷组,LVFS高于氯吡格雷组(P＜0.05)。结论 冠心宁可改善急性心肌梗死后心力衰竭大鼠心肌超微结构与心功能,降低氧化应激水平及炎症反应,其作用机制可能与激活P13K/AKT信号通路、增强线粒体功能有关。 |
| 英文摘要: |
| Objective To observe the mechanism of Guanxinning in treating heart failure rats after acute myocardial infarction. Methods The heart failure model of rats after acute myocardial infarction was established by ligating the anterior descending branch of the left coronary artery. The 45 rats with successful model were randomly divided into blank control group, clopidogrel group and Guanxinning group, with 15 rats in each group. After 4 weeks of intragastric administration, observe the changes of myocardial ultrastructure of rats in each group, detect the expression of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) in myocardial tissue, oxidative stress factor [ROS, T-AOC] in myocardial tissue, and serum tumor necrosis factor- α (TNF- α)、 Transforming growth factor- β 1(TGF- β 1) Cardiac color Doppler index [left ventricular septal systolic thickness (IVSs), left ventricular septal diastolic thickness (IVSd), left ventricular short axis shortening rate (LVFS)]. Results The heart failure model of rats after acute myocardial infarction was established by ligating the anterior descending branch of the left coronary artery. The 45 rats with successful model were randomly divided into blank control group, clopidogrel group and Guanxinning group, with 15 rats in each group. After 4 weeks of intragastric administration, observe the changes of myocardial ultrastructure of rats in each group, detect the expression of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) in myocardial tissue, oxidative stress factor [ROS, T-AOC] in myocardial tissue, and serum tumor necrosis factor- α (TNF- α)、 Transforming growth factor- β 1(TGF- β 1) Cardiac color Doppler index [left ventricular septal systolic thickness (IVSs), left ventricular septal diastolic thickness (IVSd), left ventricular short axis shortening rate (LVFS)]. Conclusion Guanxinning can improve the myocardial ultrastructure and cardiac function, reduce the level of oxidative stress and inflammatory reaction in rats with heart failure after acute myocardial infarction. Its mechanism may be related to activating P13K/AKT signal pathway and enhancing mitochondrial function. |
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