AMPK/PPARα信号通路探讨芪红散对心力衰竭大鼠心肌能量代谢的影响  

Influence of Qihong San on myocardial energy metabolism in rats with heart failure:an investigation based on AMPK/PPARαsignaling pathway

作　　者：范辉[1] 翟雪芹[1] 李江 王晓峰[1] Fan Hui;Zhai Xueqin;Li Jiang;Wang Xiaofeng(Heart Center,Hospital of Traditional Chinese Medicine,Xinjiang Medical University,Urumchi 830000,China;不详)

机构地区：[1]新疆医科大学附属中医医院心脏中心,乌鲁木齐830000 [2]新疆医科大学附属中医医院急救中心,乌鲁木齐830000

出　　处：《中国循证心血管医学杂志》2025年第1期74-77,82,共5页Chinese Journal of Evidence-Based Cardiovascular Medicine

基　　金：新疆维吾尔自治区自然科学基金面上项目(2022D01C166)。

摘　　要：目的探讨芪红散对心力衰竭大鼠心肌能量代谢及腺苷酸活化蛋白激酶/过氧化物酶体增殖物激活受体α(AMPK/PPARα)信号通路的影响。方法40只SPF级SD雄性大鼠(体重200±220 g)大鼠分为四组:假手术组、模型组、芪红散组、芪红散组+AMPK抑制剂组。采用胸主动脉缩窄法制作大鼠慢性心力衰竭,经28 d给药处理后,采用心脏超声检测大鼠左室收缩末期内径(LVESD)、左室舒张末期内径(LVEDD)、左室缩短分数(LVFS)和左室射血分数(LVEF);苏木精伊红(H&E)染色检测大鼠心肌组织病理变化;马松(Masson)染色检测大鼠心肌组织纤维化程度;Western blot检测心肌组织AMPK、磷酸化AMPK(p-AMPK)和PPARα水平;酶联免疫吸附(ELISA)试剂盒检测心肌组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、三磷酸腺苷(ATP)和活性氧(ROS)水平。结果与假手术组相比,模型组LVEF、LVFS降低,LVEDD和LVESD升高,p-AMPK、PPARα、ATP和SOD水平降低,心肌纤维排列紊乱及炎性细胞浸润增多,MDA和ROS水平升高(P<0.05)。与模型组比较,芪红散组LVEF、LVFS升高,LVEDD和LVESD降低,p-AMPK、PPARα、ATP和SOD水平升高,心肌纤维排列紊乱及炎性细胞浸润缓解,MDA和ROS水平降低(P<0.05)。与芪红散组相比,芪红散+AMPK抑制剂组逆转芪红散对心力衰竭大鼠心肌细胞能量代谢及氧化损伤的调控作用。结论芪红散激活AMPK/PPARα信号通路,改善心力衰竭大鼠心肌能量代谢,减轻氧化应激损伤。Objective To investigate the influence of Qihong San on myocardial energy metabolism and signaling pathway of AMP-activated protein kinase/peroxisome proliferator-activated receptorα(AMPK/PPARα)in rats with heart failure(HF).Methods Male SD rats(SPF grade,n=40,body weigh=200±220 g)were divided into sham-operation group,model group,Qihong San group and Qihong San+AMPK inhibitor group.HF was induced by using transverse aortic constriction(TAC)in rats,and after 28 d medication treatment,and left ventricular end-systolic diameter(LVESD),left ventricular end-diastolic diameter(LVEDD),left ventricular fraction shortening(LVFS)and left ventricular ejection fraction(LVEF)were detected by using cardiac ultrasonography.The pathological changes of rat myocardial tissue were detected by using H&E staining,and myocardial fibrosis was detected by using Masson staining.The levels of AMPK,phosphorylated AMPK(p-AMPK)and PPARαwere detected by using Western blotting assay.The levels of superoxide dismutase(SOD),malondialdehyde(MDA),adenosine triphosphate(ATP)and reactive oxygen species(ROS)were detected by using enzyme-linked immunosorbent assay(ELISA).Results Compared with sham-operation group,LVEF and LVFS decreased,LVEDD and LVESD increased,levels of p-AMPK,PPARα,ATP and SOD decreased,disorderof myocardial fiber arrangement and inflammatory cell infiltrationincreased,and levels of MDA and ROS increased in model group(P<0.05).Compared with model group,LVEF and LVFS increased,LVEDD and LVESD decreased,levels of p-AMPK,PPARα,ATP and SOD increased,disorderof myocardial fiber arrangement and inflammatory cell infiltrationwere relieved,and levels of MDA and ROS decreased in Qihong San group(P<0.05).Compared with Qihong San group,the regulative effects of Qihong San on myocardial energy metabolism and oxidative damage were reversed in Qihong San+AMPK inhibitor group.Conclusion Qihong San can activite AMPK/PPARαsignaling pathway,improve myocardial energy metabolism and relieve oxidative damage in HF rats.

关 键 词：心肌能量代谢 芪红散 氧化损伤 AMPK/PPARα 大鼠 

分 类 号：R28[医药卫生—中药学]