Effect of ginsenoside Rb3 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 4 groups: 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 2 mL · kg-1 · d-1i.p). The rats in G-Rb3 group were treated with G-Rb3 (with 20 mg · kg-1 · d-1 i.p). The rats in captopril group was treated with captopril (100 mg · kg-1 · d-1 i.g). After 4 weeks, 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), angiotensin II (AngII) in plasma, myocardial angiotensin II (Ang II) were determined. Results: Compared with model group, the cardiac coefficient, the left ventricular end diastolic pressure (LVEDP) were decreased significantly (P<0.01), the mean arterial blood pressure(MAP) and the maximum left ventricular presure rising and dropping rates(± dp/dtmax) were increased significantly in G-Rb3group (P<0.01). In addition, Compared with model group,the contents of MDA in serum, ET, Ang II in plasma and myocardial Ang II were declined (P<0.01), then the activities of SOD and GSH-Px in serum were increased markedly in G-Rb3 group (P<0.01). Conclusion: G-Rb3 has protective effect on ventricular remodeling through inhibitting renin-angiotensin-aldosterone system (RAAS) to reduce contractive material and reinforcing ability of anti-oxidant. (authors)