Role of hesperetin intervention on cardiac function and ventricular remodeling after myocardial infarction / 中华急诊医学杂志

ABSTRACT

Objective To explore the effect of hesperidin on cardiac function and ventricular remodeling following myocardial infarction (MI) in mice.Methods Ligation of left anterior descending (LAD) was operated to establish MI model.Forty-two C57BL/6 mice were randomly (random number) divided into control and MI group;and 24 h after LAD ligation,mice in MI group were further divided into MI control and hesperetin group.Eight weeks later,cardiac function and structure changes were determined by the methods of hemodynamic measurement and echocardiography.HE staining was used to measure crosssectional area (CSA) of atrial myocytes,and PSR staining was applied for observe collagen deposition and calculation of collagen volume fraction (CVF).Real-time PCR was used to detect the mRNA expressions of cardiac hypertrophy markers (ANP,BNP and β-MHC) and cardiac fibrosis markers (Collagen Ⅰ,Collagen Ⅲ and CTGF).The contents of superoxide anion and hydroxy radical were detected by colorimetric method.Results Compared with control group,left ventricular posterior wall thickness (LVPWT) and interventricular septum thickness (IVST) were increased to be thicker,left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) were significantly lower,and ± dp/dtmax was remarkably reduced in MI control group (P ＜ 0.05).Compared with MI control group,hesperetin could increaseLVFS [(29.48±3.87)％ vs.(20.69±3.99) ％],LVEF [(46.40±1.68)％ vs.(30.51± 1.17) ％] and ±dp/dtmax [(3 344.33 ±269.57) mmHg/S vs.(2 205.19 ±224.17) mmHg/S;(2250.40±218.35) mmHg/S vs.(-1 566.91 ±217.37) mmHg/S];but could reduce LVPWT [(2.29±0.05) mm vs.(2.85±0.10)mm]andIVST[(1.44±0.09) mm vs.(1.89±0.06) mm].Compared with control group,CSA and CVF were significantly increased in MI control mice.However,hesperetin could reduce CSA and CVF.Compared with control group,the mRNA expressions of cardiac hypertrophy and cardiac fibrosis markers were significantly increased in MI control mice;but hesperetin could significantly inhibit the mRNA expressions of cardiac hypertrophy and cardiac fibrosis markers.Additionally,hesperetin could significantly reduce the contents of superoxide anion and hydroxy radical.Conclusion Hesperetin intervention can inhibit ventricular structure change,and improve hemodynamics and cardiac function after acute myocardial infarction via inhibiting the production of reactive oxygen species (ROS).