Effect of ginsenoside Rb 3 on experimental ventricular remodeling in rats and its mechanism

Objective To study the effect of ginsenoside Rb3 (G-Rb3)on experimental ventricular remodeling in rats and investigate its mechanism.Methods The ventricular remodeling model was induced by myocardial infarction in rats of left anterior descending coronary occulusion.The Wistar rats were divided into 4groups:sham operation group,remodeling model group,G-Rb3 group,and captopril group.The rats in sham operation group and remodeling model group were treated with normal sodium (with 2mL·kg-1·d-1i.p).The rats in G-Rb3group were treated with G-Rb3 (with 20mg·kg-1·d-1 i.p).The rats in captopril group was treated with captopril (100mg·kg-1·d-1 i.g).After 4weeks,the morphological parameters,histopathology,hemodynamic changes, biochemical analysis were determined in rats.The content of malondialdehyde(MDA)in serum and activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px)in plasma,the content of endothelin (ET), angiotensinⅡ (AngⅡ)in plasma,myocardial angiotensinⅡ (AngⅡ)were determined.Results Compared with model group,the cardiac coefficient,the left ventricular end diastolic pressure (LVEDP)weredecreasedsignificantly(P0.01),the mean arterial blood pressure(MAP)and the maximum left ventricular presure rising and dropping rates(±dp/dtmax)were increased significantly in G-Rb3group (P0.01).In addition,Compared with model group,the contents of MDA in serum,ET,AngⅡin plasma and myocardial AngⅡ were declined (P0.01),then the activities of SOD and GSH-Px in serum were increased markedly in G-Rb3group (P0.01). Conclusion G-Rb3has protective effect on ventricular remodeling through inhibitting renin-angiotensin-aldosterone system (RAAS)to reduce contractive material and reinforcing ability of anti-oxidant.