Effects of ginsenoside Rb1 on serum brain natriuretic peptide level and caspase-3 protein expression in cardiomyocytes of rats with chronic heart failure

Abstract

Context: Ginsenoside Rb1 is a representative ginsenoside, and caspase-3 is implicated in chronic heart failure (CHF). Aim: The aim of this study was to evaluate the effects of ginsenoside Rb1 on the level of brain natriuretic peptide (BNP) in serum and the expression of caspase-3 protein in the cardiomyocytes of CHF rats. Subjects and Methods: A total of 48 Wistar rats were divided into control, model, positive control (losartan), and ginsenoside Rb1 groups at random (n = 12). Abdominal aortic constriction was adopted for CHF modeling. Four weeks after surgery, ginsenoside Rb1 and losartan groups were intragastrically administered with 50 mg/kg ginsenoside Rb1 and 4.5 mg/kg losartan daily, respectively. Control and model groups were given equal volumes of distilled water. Cardiac function indices, electrocardiographic signals, BNP level, heart weight, body weight, heart-to-body weight ratio, myocardial pathological changes, and caspase-3 protein expression were compared. Results: In contrast to model group, heart rate, left ventricular end-diastolic pressure, BNP level, and caspase-3 protein expression of ginsenoside Rb1 and losartan groups notably dropped, whereas left ventricular systolic pressure and maximal rise/fall rate of the left ventricular pressure significantly rose (P < 0.05). The heart weight and heart-to-body weight ratio of ginsenoside Rb1 and losartan groups were evidently lower relative to those in the model group (P < 0.05). The ST segments of losartan and ginsenoside Rb1 groups fell after rise. Ginsenoside Rb1 inhibited focal cardiomyocyte necrosis and steatosis and relieved myocardial myofibrillar dissolution. It evidently decreased broken muscle bundles, as well as alleviated fibrosis and myocardial fibrosis. Conclusion: Ginsenoside Rb1 can improve the cardiac function of CHF rats, probably by inhibiting the apoptosis of cardiomyocytes.